https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and >clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some >arbitrary length of protein coding sequence to remove noise due to open >reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could >determine had an evolutionary history (conserved from ancestral de novo >creation of the gene). They did knockout gene analysis and created >nonfunctional copies in cell culture and found that 44 of them that >significantly affected the cells in cell culture and had a measurable >fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <rokimoto@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
On 12/27/2022 1:14 AM, jillery wrote:
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <rokimoto@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the >micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <rokimoto@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <rokimoto@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and >>>> clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open >>>> reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo >>>> creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >>>> think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo >>from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
OK, that says to me the new gene isn't technically "de novo" in the
sense that Behe means of being purposefully designed.
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and >>> clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open >>> reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo >>> creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >>> think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the >micro protein, and the sequence had to evolve the transcriptional >regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron OkimotoOK, that says to me the new gene isn't technically "de novo" in the
sense that Behe means of being purposefully designed.
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and >> >>> clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open >> >>> reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo >> >>> creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable >> >>> fitness effect.
19 short ORF with measurable fitness effects had an origin within the >> >>> last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >> >>> think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes >> >>> that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that >> >> would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated >> >by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and >>>>> clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some >>>>> arbitrary length of protein coding sequence to remove noise due to open >>>>> reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could >>>>> determine had an evolutionary history (conserved from ancestral de novo >>>>> creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable >>>>> fitness effect.
19 short ORF with measurable fitness effects had an origin within the >>>>> last 43 million years of primate evolution. 2 of the short ORF genes >>>>> with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >>>>> think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes >>>>> that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that >>>> would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated >>> by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and >>>>>> clicking on the DOI.
This is a paper that looked at short open reading frames. These are >>>>>> usually missed in most functional analyses because we often put some >>>>>> arbitrary length of protein coding sequence to remove noise due to open >>>>>> reading frames (ORF) that just happen by chance in random sequence. >>>>>> This paper tracked down 144 of these short ORF genes that they could >>>>>> determine had an evolutionary history (conserved from ancestral de novo >>>>>> creation of the gene). They did knockout gene analysis and created >>>>>> nonfunctional copies in cell culture and found that 44 of them that >>>>>> significantly affected the cells in cell culture and had a measurable >>>>>> fitness effect.
19 short ORF with measurable fitness effects had an origin within the >>>>>> last 43 million years of primate evolution. 2 of the short ORF genes >>>>>> with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >>>>>> think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >>>>>>
Behe should likely be looking for his IC mutations in these new genes >>>>>> that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that >>>>> would contradict the authors claim that they tracked the origins back >>>>> to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the >>>> micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated >>>> by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
The place holder sequence would have to change over time while keeping >enough of the sequence the same so that it could be determined that
there was place holder sequence there at one time that changed into a >functional gene.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell >culture, the ID perps would claim that they were designed to fulfill the >purpose that they now have. They were designed by an evolutionary
process, but that doesn't seem to matter for ID perps like Behe. Behe >understands that biological evolution is a fact of nature. He just
thinks that the designer has something to do with getting the right >mutations into the sequence at the right time to create the evolution
that has been observed.
On Thu, 29 Dec 2022 16:42:26 -0800 (PST), Robert Carnegie <rja.ca...@excite.com> wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some >> >>> arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could >> >>> determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable >> >>> fitness effect.
19 short ORF with measurable fitness effects had an origin within the >> >>> last 43 million years of primate evolution. 2 of the short ORF genes >> >>> with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >> >>> think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes >> >>> that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that >> >> would contradict the authors claim that they tracked the origins back >> >> to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the >> >micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated >> >by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Perhaps "we" aren't, but Behe and other cdesign proponentsists are.
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and >>>>> clicking on the DOI.
This is a paper that looked at short open reading frames. These are >>>>> usually missed in most functional analyses because we often put some >>>>> arbitrary length of protein coding sequence to remove noise due to open >>>>> reading frames (ORF) that just happen by chance in random sequence. >>>>> This paper tracked down 144 of these short ORF genes that they could >>>>> determine had an evolutionary history (conserved from ancestral de novo >>>>> creation of the gene). They did knockout gene analysis and created >>>>> nonfunctional copies in cell culture and found that 44 of them that >>>>> significantly affected the cells in cell culture and had a measurable >>>>> fitness effect.
19 short ORF with measurable fitness effects had an origin within the >>>>> last 43 million years of primate evolution. 2 of the short ORF genes >>>>> with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >>>>> think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >>>>>
Behe should likely be looking for his IC mutations in these new genes >>>>> that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that >>>> would contradict the authors claim that they tracked the origins back >>>> to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the >>> micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated >>> by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not meanThe place holder sequence would have to change over time while keeping
that He wouldn't.
enough of the sequence the same so that it could be determined that
there was place holder sequence there at one time that changed into a functional gene.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell culture, the ID perps would claim that they were designed to fulfill the purpose that they now have. They were designed by an evolutionary
process, but that doesn't seem to matter for ID perps like Behe. Behe understands that biological evolution is a fact of nature. He just
thinks that the designer has something to do with getting the right
mutations into the sequence at the right time to create the evolution
that has been observed.
On Friday, 30 December 2022 at 07:45:35 UTC, jillery wrote:
On Thu, 29 Dec 2022 16:42:26 -0800 (PST), Robert Carnegie
<rja.ca...@excite.com> wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are >> >> >>> usually missed in most functional analyses because we often put some >> >> >>> arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence. >> >> >>> This paper tracked down 144 of these short ORF genes that they could >> >> >>> determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created >> >> >>> nonfunctional copies in cell culture and found that 44 of them that >> >> >>> significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes >> >> >>> with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >> >> >>>
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back >> >> >> to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo >> >> >from non coding sequence. The open reading frame evolved to produce the >> >> >micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding >> >> >DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start >> >> >codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Perhaps "we" aren't, but Behe and other cdesign proponentsists are.
Are they discussing real genes that were purposefully
designed? I'm presuming no and no. Genes are only
purposefully designed in a laboratory, and mostly not
even that, but by copying. I think copying, such as in
mRNA vaccines, doesn't amount to design.
On Fri, 30 Dec 2022 04:56:39 -0600, RonO <rokimoto@cox.net> wrote:
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and >>>>>>> clicking on the DOI.
This is a paper that looked at short open reading frames. These are >>>>>>> usually missed in most functional analyses because we often put some >>>>>>> arbitrary length of protein coding sequence to remove noise due to open >>>>>>> reading frames (ORF) that just happen by chance in random sequence. >>>>>>> This paper tracked down 144 of these short ORF genes that they could >>>>>>> determine had an evolutionary history (conserved from ancestral de novo >>>>>>> creation of the gene). They did knockout gene analysis and created >>>>>>> nonfunctional copies in cell culture and found that 44 of them that >>>>>>> significantly affected the cells in cell culture and had a measurable >>>>>>> fitness effect.
19 short ORF with measurable fitness effects had an origin within the >>>>>>> last 43 million years of primate evolution. 2 of the short ORF genes >>>>>>> with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >>>>>>> think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >>>>>>>
Behe should likely be looking for his IC mutations in these new genes >>>>>>> that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would >>>>>> contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that >>>>>> would contradict the authors claim that they tracked the origins back >>>>>> to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo >>>> >from non coding sequence. The open reading frame evolved to produce the >>>>> micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated >>>>> by the ribosomes. The sequence existed in some ancestor as non coding >>>>> DNA, but mutations had to happen to get it transcribed and for it to >>>>> encode the amino acid sequence of the microprotein. It needed a start >>>>> codon and a termination codon, and a protein sequence that fulfilled >>>>> some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
The place holder sequence would have to change over time while keeping
enough of the sequence the same so that it could be determined that
there was place holder sequence there at one time that changed into a
functional gene.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell
culture, the ID perps would claim that they were designed to fulfill the
purpose that they now have. They were designed by an evolutionary
process, but that doesn't seem to matter for ID perps like Behe. Behe
understands that biological evolution is a fact of nature. He just
thinks that the designer has something to do with getting the right
mutations into the sequence at the right time to create the evolution
that has been observed.
IIUC your description above severely understates Behe's expressed disagreement about mutations. All of his books and lectures about ID
assert a common theme, that the "right" mutations are just too
improbable to have happened by unguided natural processes. That's why
he presumes a purposeful designer, to force the creation of those
"right" mutations that would not and could not have happened at the
right time and place and sequence. That's very different from your description above, which implies that the "right" mutations appeared
just *as if* they were caused by unguided natural processes but *in
fact* God purposely made them appear that way. If that was Behe's
claim, he would have utterly no basis for claiming that unguided
natural processes are insufficient to explain the diversity (and
disparity) of life on Earth.
On 12/30/2022 6:40 AM, jillery wrote:
On Fri, 30 Dec 2022 04:56:39 -0600, RonO <rokimoto@cox.net> wrote:
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote: >>>>>>>
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are >>>>>>>> usually missed in most functional analyses because we often put some >>>>>>>> arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence. >>>>>>>> This paper tracked down 144 of these short ORF genes that they could >>>>>>>> determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created >>>>>>>> nonfunctional copies in cell culture and found that 44 of them that >>>>>>>> significantly affected the cells in cell culture and had a measurable >>>>>>>> fitness effect.
19 short ORF with measurable fitness effects had an origin within the >>>>>>>> last 43 million years of primate evolution. 2 of the short ORF genes >>>>>>>> with measurable fitness effects were found to have evolved from >>>>>>>> noncoding sequence since the human lineage separated from chimps. They >>>>>>>> think that such new genes might have an important effect in the >>>>>>>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >>>>>>>>
Behe should likely be looking for his IC mutations in these new genes >>>>>>>> that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have >>>>>>> recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would >>>>>>> contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that >>>>>>> would contradict the authors claim that they tracked the origins back >>>>>>> to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo >>>>> >from non coding sequence. The open reading frame evolved to produce the >>>>>> micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated >>>>>> by the ribosomes. The sequence existed in some ancestor as non coding >>>>>> DNA, but mutations had to happen to get it transcribed and for it to >>>>>> encode the amino acid sequence of the microprotein. It needed a start >>>>>> codon and a termination codon, and a protein sequence that fulfilled >>>>>> some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
The place holder sequence would have to change over time while keeping
enough of the sequence the same so that it could be determined that
there was place holder sequence there at one time that changed into a
functional gene.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell
culture, the ID perps would claim that they were designed to fulfill the >>> purpose that they now have. They were designed by an evolutionary
process, but that doesn't seem to matter for ID perps like Behe. Behe
understands that biological evolution is a fact of nature. He just
thinks that the designer has something to do with getting the right
mutations into the sequence at the right time to create the evolution
that has been observed.
IIUC your description above severely understates Behe's expressed
disagreement about mutations. All of his books and lectures about ID
assert a common theme, that the "right" mutations are just too
improbable to have happened by unguided natural processes. That's why
he presumes a purposeful designer, to force the creation of those
"right" mutations that would not and could not have happened at the
right time and place and sequence. That's very different from your
description above, which implies that the "right" mutations appeared
just *as if* they were caused by unguided natural processes but *in
fact* God purposely made them appear that way. If that was Behe's
claim, he would have utterly no basis for claiming that unguided
natural processes are insufficient to explain the diversity (and
disparity) of life on Earth.
This seems to be just restating what I wrote. "Behe understands that >biological evolution is a fact of nature. He just thinks that the
designer has something to do with getting the right mutations into the >sequence at the right time to create the evolution that has been observed."
Behe thinks that his IC systems needed Designer help to get the right >mutations in the right place within the time that it took. He has >repeatedly claimed that one of his criteria is that it is impossible to
get the needed mutations that he claims exists that created his systems
in the time that was available. It is why he put up his "waiting time" >argument claiming that populations of a given size would be unable to
create his two neutral mutations to produce a given function within some >reasonable time frame. He just doesn't have any evidence that his type
of evolution ever occurred in the populations that he claims that they
would be unlikely to occur in. He knows that 2 neutral mutations would >routinely occur to produce a given function (if it were possible) in the >populations that evolved his IC systems because the population sizes
were likely greater than a trillion at any given time when the flagellum
was evolving or blood clotting and the adaptive immune system, so he had
to go with 3 neutral mutations to produce a function, but we have never >identified any such thing ever occurring, and Behe pretty much refuses
to look for them. The population limit applies to lineages like the ape >lineage or the elephant lineage where the likely in the hundreds of >thousands to millions at most. We have never identified Behe's two
neutral mutations in such lineages, but Thornton did find 2 neutral >mutations involved in the change of ligand binding for steroid
receptors, but that evolution occurred before multicellular animals
evolved and the cell populations were likely large enough to have such a >thing occur routinely. The limitation was likely if the rest of the >cellular functions were ready to take advantage of the mutations so that
the new function could be selected for once the mutations had occurred.
Ron Okimoto
On Fri, 30 Dec 2022 06:45:54 -0800 (PST), Robert Carnegie <rja.ca...@excite.com> wrote:
On Friday, 30 December 2022 at 07:45:35 UTC, jillery wrote:
On Thu, 29 Dec 2022 16:42:26 -0800 (PST), Robert Carnegie
<rja.ca...@excite.com> wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are >> >> >>> usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence. >> >> >>> This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created >> >> >>> nonfunctional copies in cell culture and found that 44 of them that >> >> >>> significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >> >> >>>
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would >> >> >> contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo >> >> >from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding >> >> >DNA, but mutations had to happen to get it transcribed and for it to >> >> >encode the amino acid sequence of the microprotein. It needed a start >> >> >codon and a termination codon, and a protein sequence that fulfilled >> >> >some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Perhaps "we" aren't, but Behe and other cdesign proponentsists are.
Are they discussing real genes that were purposefully
designed? I'm presuming no and no. Genes are only
purposefully designed in a laboratory, and mostly not
even that, but by copying. I think copying, such as in
mRNA vaccines, doesn't amount to design.
As you should know, "they" use a different meaning of "purposefully
designed" than you and I do.
On Friday, 30 December 2022 at 16:05:35 UTC, jillery wrote:
On Fri, 30 Dec 2022 06:45:54 -0800 (PST), Robert Carnegie
<rja.ca...@excite.com> wrote:
On Friday, 30 December 2022 at 07:45:35 UTC, jillery wrote:
On Thu, 29 Dec 2022 16:42:26 -0800 (PST), Robert Carnegie
<rja.ca...@excite.com> wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the >> >> >> sense that Behe means of being purposefully designed.
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote: >> >> >> >>
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from >> >> >> >>> noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the >> >> >> >>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have >> >> >> >> recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would >> >> >> >> contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to >> >> >> >encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled >> >> >> >some new function.
Ron Okimoto
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Perhaps "we" aren't, but Behe and other cdesign proponentsists are.
Are they discussing real genes that were purposefully
designed? I'm presuming no and no. Genes are only
purposefully designed in a laboratory, and mostly not
even that, but by copying. I think copying, such as in
mRNA vaccines, doesn't amount to design.
As you should know, "they" use a different meaning of "purposefully
designed" than you and I do.
Do you mean they're lying? That, I do know.
Should I really know what they mean, other than
that they mean to deceive?
On Fri, 30 Dec 2022 19:53:14 -0600, RonO <rokimoto@cox.net> wrote:
On 12/30/2022 6:40 AM, jillery wrote:
On Fri, 30 Dec 2022 04:56:39 -0600, RonO <rokimoto@cox.net> wrote:
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the >>>>>> sense that Behe means of being purposefully designed.
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are >>>>>>>>> usually missed in most functional analyses because we often put some >>>>>>>>> arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence. >>>>>>>>> This paper tracked down 144 of these short ORF genes that they could >>>>>>>>> determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created >>>>>>>>> nonfunctional copies in cell culture and found that 44 of them that >>>>>>>>> significantly affected the cells in cell culture and had a measurable >>>>>>>>> fitness effect.
19 short ORF with measurable fitness effects had an origin within the >>>>>>>>> last 43 million years of primate evolution. 2 of the short ORF genes >>>>>>>>> with measurable fitness effects were found to have evolved from >>>>>>>>> noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the >>>>>>>>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >>>>>>>>>
Behe should likely be looking for his IC mutations in these new genes >>>>>>>>> that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have >>>>>>>> recently originated entirely de novo from noncoding sequences" >>>>>>>>
If the authors mean to say the *functions* are de novo, that would >>>>>>>> contradict Behe's claim that functional novelty appears rarely. >>>>>>>>
OTOH if the authors mean to say the genes themselves are de novo, that >>>>>>>> would contradict the authors claim that they tracked the origins back >>>>>>>> to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo >>>>>> >from non coding sequence. The open reading frame evolved to produce the >>>>>>> micro protein, and the sequence had to evolve the transcriptional >>>>>>> regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding >>>>>>> DNA, but mutations had to happen to get it transcribed and for it to >>>>>>> encode the amino acid sequence of the microprotein. It needed a start >>>>>>> codon and a termination codon, and a protein sequence that fulfilled >>>>>>> some new function.
Ron Okimoto
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
The place holder sequence would have to change over time while keeping >>>> enough of the sequence the same so that it could be determined that
there was place holder sequence there at one time that changed into a
functional gene.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell
culture, the ID perps would claim that they were designed to fulfill the >>>> purpose that they now have. They were designed by an evolutionary
process, but that doesn't seem to matter for ID perps like Behe. Behe >>>> understands that biological evolution is a fact of nature. He just
thinks that the designer has something to do with getting the right
mutations into the sequence at the right time to create the evolution
that has been observed.
IIUC your description above severely understates Behe's expressed
disagreement about mutations. All of his books and lectures about ID
assert a common theme, that the "right" mutations are just too
improbable to have happened by unguided natural processes. That's why
he presumes a purposeful designer, to force the creation of those
"right" mutations that would not and could not have happened at the
right time and place and sequence. That's very different from your
description above, which implies that the "right" mutations appeared
just *as if* they were caused by unguided natural processes but *in
fact* God purposely made them appear that way. If that was Behe's
claim, he would have utterly no basis for claiming that unguided
natural processes are insufficient to explain the diversity (and
disparity) of life on Earth.
This seems to be just restating what I wrote. "Behe understands that
biological evolution is a fact of nature. He just thinks that the
designer has something to do with getting the right mutations into the
sequence at the right time to create the evolution that has been observed."
There's a difference between claiming "right mutations" are too
improbable without a purposeful intelligent agent, and claiming that a purposeful intelligent agent just happened to decide the way "right mutations" would have happened all by themselves anyway. The latter
is just a version of shooting an arrow and then drawing a target
around whatever it hit, and would not support the claims and
conclusions Behe makes.
Behe thinks that his IC systems needed Designer help to get the right
mutations in the right place within the time that it took. He has
repeatedly claimed that one of his criteria is that it is impossible to
get the needed mutations that he claims exists that created his systems
in the time that was available. It is why he put up his "waiting time"
argument claiming that populations of a given size would be unable to
create his two neutral mutations to produce a given function within some
reasonable time frame. He just doesn't have any evidence that his type
of evolution ever occurred in the populations that he claims that they
would be unlikely to occur in. He knows that 2 neutral mutations would
routinely occur to produce a given function (if it were possible) in the
populations that evolved his IC systems because the population sizes
were likely greater than a trillion at any given time when the flagellum
was evolving or blood clotting and the adaptive immune system, so he had
to go with 3 neutral mutations to produce a function, but we have never
identified any such thing ever occurring, and Behe pretty much refuses
to look for them. The population limit applies to lineages like the ape
lineage or the elephant lineage where the likely in the hundreds of
thousands to millions at most. We have never identified Behe's two
neutral mutations in such lineages, but Thornton did find 2 neutral
mutations involved in the change of ligand binding for steroid
receptors, but that evolution occurred before multicellular animals
evolved and the cell populations were likely large enough to have such a
thing occur routinely. The limitation was likely if the rest of the
cellular functions were ready to take advantage of the mutations so that
the new function could be selected for once the mutations had occurred.
Ron Okimoto
On Friday, 30 December 2022 at 11:00:35 UTC, Ron O wrote:
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:The place holder sequence would have to change over time while keeping
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and >>>>>>> clicking on the DOI.
This is a paper that looked at short open reading frames. These are >>>>>>> usually missed in most functional analyses because we often put some >>>>>>> arbitrary length of protein coding sequence to remove noise due to open >>>>>>> reading frames (ORF) that just happen by chance in random sequence. >>>>>>> This paper tracked down 144 of these short ORF genes that they could >>>>>>> determine had an evolutionary history (conserved from ancestral de novo >>>>>>> creation of the gene). They did knockout gene analysis and created >>>>>>> nonfunctional copies in cell culture and found that 44 of them that >>>>>>> significantly affected the cells in cell culture and had a measurable >>>>>>> fitness effect.
19 short ORF with measurable fitness effects had an origin within the >>>>>>> last 43 million years of primate evolution. 2 of the short ORF genes >>>>>>> with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They >>>>>>> think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >>>>>>>
Behe should likely be looking for his IC mutations in these new genes >>>>>>> that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would >>>>>> contradict Behe's claim that functional novelty appears rarely.
OTOH if the authors mean to say the genes themselves are de novo, that >>>>>> would contradict the authors claim that they tracked the origins back >>>>>> to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo >>>> >from non coding sequence. The open reading frame evolved to produce the >>>>> micro protein, and the sequence had to evolve the transcriptional
regulatory sequences needed to transcribe the gene and get it translated >>>>> by the ribosomes. The sequence existed in some ancestor as non coding >>>>> DNA, but mutations had to happen to get it transcribed and for it to >>>>> encode the amino acid sequence of the microprotein. It needed a start >>>>> codon and a termination codon, and a protein sequence that fulfilled >>>>> some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
enough of the sequence the same so that it could be determined that
there was place holder sequence there at one time that changed into a
functional gene.
So, maybe God puts in a noncoding rough sketch
of the gene that He eventually will put there, so that
He doesn't forget? ;-)
But in fact, while I don't understand most of this matter,Since these new genes were determined to have fitness effects in cell
I am confident that we aren't discussing a gene that was
purposefully designed.
culture, the ID perps would claim that they were designed to fulfill the
purpose that they now have. They were designed by an evolutionary
process, but that doesn't seem to matter for ID perps like Behe. Behe
understands that biological evolution is a fact of nature. He just
thinks that the designer has something to do with getting the right
mutations into the sequence at the right time to create the evolution
that has been observed.
I don't play this game at your level in any sense, but
I don't like the word "design" referring to a natural
process of evolution. I consider it concedes too
much, like saying that a stream flows downhill
by design. No, it just happened.
On 12/31/2022 3:37 AM, jillery wrote:
On Fri, 30 Dec 2022 19:53:14 -0600, RonO <rokimoto@cox.net> wrote:
On 12/30/2022 6:40 AM, jillery wrote:
On Fri, 30 Dec 2022 04:56:39 -0600, RonO <rokimoto@cox.net> wrote:
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote: >>>>>>>
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the >>>>>>> sense that Behe means of being purposefully designed.
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>>
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are >>>>>>>>>> usually missed in most functional analyses because we often put some >>>>>>>>>> arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence. >>>>>>>>>> This paper tracked down 144 of these short ORF genes that they could >>>>>>>>>> determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created >>>>>>>>>> nonfunctional copies in cell culture and found that 44 of them that >>>>>>>>>> significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes >>>>>>>>>> with measurable fitness effects were found to have evolved from >>>>>>>>>> noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the >>>>>>>>>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >>>>>>>>>>
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have >>>>>>>>> recently originated entirely de novo from noncoding sequences" >>>>>>>>>
If the authors mean to say the *functions* are de novo, that would >>>>>>>>> contradict Behe's claim that functional novelty appears rarely. >>>>>>>>>
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back >>>>>>>>> to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo >>>>>>> >from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional >>>>>>>> regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding >>>>>>>> DNA, but mutations had to happen to get it transcribed and for it to >>>>>>>> encode the amino acid sequence of the microprotein. It needed a start >>>>>>>> codon and a termination codon, and a protein sequence that fulfilled >>>>>>>> some new function.
Ron Okimoto
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-) >>>>>>
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
The place holder sequence would have to change over time while keeping >>>>> enough of the sequence the same so that it could be determined that
there was place holder sequence there at one time that changed into a >>>>> functional gene.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell >>>>> culture, the ID perps would claim that they were designed to fulfill the >>>>> purpose that they now have. They were designed by an evolutionary
process, but that doesn't seem to matter for ID perps like Behe. Behe >>>>> understands that biological evolution is a fact of nature. He just
thinks that the designer has something to do with getting the right
mutations into the sequence at the right time to create the evolution >>>>> that has been observed.
IIUC your description above severely understates Behe's expressed
disagreement about mutations. All of his books and lectures about ID
assert a common theme, that the "right" mutations are just too
improbable to have happened by unguided natural processes. That's why >>>> he presumes a purposeful designer, to force the creation of those
"right" mutations that would not and could not have happened at the
right time and place and sequence. That's very different from your
description above, which implies that the "right" mutations appeared
just *as if* they were caused by unguided natural processes but *in
fact* God purposely made them appear that way. If that was Behe's
claim, he would have utterly no basis for claiming that unguided
natural processes are insufficient to explain the diversity (and
disparity) of life on Earth.
This seems to be just restating what I wrote. "Behe understands that
biological evolution is a fact of nature. He just thinks that the
designer has something to do with getting the right mutations into the
sequence at the right time to create the evolution that has been observed." >>
There's a difference between claiming "right mutations" are too
improbable without a purposeful intelligent agent, and claiming that a
purposeful intelligent agent just happened to decide the way "right
mutations" would have happened all by themselves anyway. The latter
is just a version of shooting an arrow and then drawing a target
around whatever it hit, and would not support the claims and
conclusions Behe makes.
Behe is obviously claiming both.
His argument is that if his 3 neutral
mutations did occur in his IC systems that they would not have occurred
in a reasonable time without designer assistance. So he makes both
claims. If it is nearly impossible for something to have happened by >natural mechanisms, his designer must have done it.
Behe really does
claim that his designer tweeks things as life has evolved on this
planet. Behe's designer takes genes that already exist and makes sure
that the right mutations occur at the right time to evolve the new
function. He acknowledges that research like Thornton's on the steroid >receptor genes is valid and that Thornton was able to recreate the
ancestral protein sequence and determine that 2 neutral mutations
occurred to create the new ligand binding capacity that created a whole
new family of steroid receptors. Behe even acknowledged that 2 neutral >mutations could have evolved by natural known mechanisms, he only
denigrated the finding by claiming that his designer could have done
better, and that his designer would be needed to put in 3 neutral
mutations to create a new function. No one has ever identified such an >example, but Behe really tries to denigrate Thornton's findings by
claiming that 2 neutral mutations are on the "edge of evolution" in
that, that is as far as natural mechanisms can be expected to go in
terms of the evolution of life on earth. Behe really is claiming that
his designer is involved in the tweeking to evolve things past the
boundary that he has created in his mind. It is still biological
evolution, but with designer assistance.
Just think about Behe's whale devolution and evolution by breaking
things stupidity. Behe really does claim that natural "Darwinian" >mechanisms can account for the whale evolution that we have figured out
so far. He calls it evolution by breaking things because a terrestrial >mammal that had evolved for a couple hundred million years adapting to
life on land and to make the transition back to the water. It is a
really stupid creationist argument because Behe is claiming that whales >could have evolved when the designer wasn't looking, and that it was >evolution so bad that his designer didn't have to be involved. Behe
claims that his designer was needed to do the really nifty things like >design his IC systems. The flagellum evolved over a billion years ago,
the blood clotting and adaptive immune systems evolved around half a
billion years ago. The aquatic ancestors of whales had these systems
before the tried to make a living on dry land, and whales took these IC >systems back into the water with them. Systems that they had inherited
from their ancestors.
Behe thinks that his IC systems needed Designer help to get the right
mutations in the right place within the time that it took. He has
repeatedly claimed that one of his criteria is that it is impossible to
get the needed mutations that he claims exists that created his systems
in the time that was available. It is why he put up his "waiting time"
argument claiming that populations of a given size would be unable to
create his two neutral mutations to produce a given function within some >>> reasonable time frame. He just doesn't have any evidence that his type
of evolution ever occurred in the populations that he claims that they
would be unlikely to occur in. He knows that 2 neutral mutations would
routinely occur to produce a given function (if it were possible) in the >>> populations that evolved his IC systems because the population sizes
were likely greater than a trillion at any given time when the flagellum >>> was evolving or blood clotting and the adaptive immune system, so he had >>> to go with 3 neutral mutations to produce a function, but we have never
identified any such thing ever occurring, and Behe pretty much refuses
to look for them. The population limit applies to lineages like the ape >>> lineage or the elephant lineage where the likely in the hundreds of
thousands to millions at most. We have never identified Behe's two
neutral mutations in such lineages, but Thornton did find 2 neutral
mutations involved in the change of ligand binding for steroid
receptors, but that evolution occurred before multicellular animals
evolved and the cell populations were likely large enough to have such a >>> thing occur routinely. The limitation was likely if the rest of the
cellular functions were ready to take advantage of the mutations so that >>> the new function could be selected for once the mutations had occurred.
Ron Okimoto
On Sat, 31 Dec 2022 07:56:17 -0600, RonO <rokimoto@cox.net> wrote:
On 12/31/2022 3:37 AM, jillery wrote:
On Fri, 30 Dec 2022 19:53:14 -0600, RonO <rokimoto@cox.net> wrote:
On 12/30/2022 6:40 AM, jillery wrote:
On Fri, 30 Dec 2022 04:56:39 -0600, RonO <rokimoto@cox.net> wrote:
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the >>>>>>>> sense that Behe means of being purposefully designed.
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>>>
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are >>>>>>>>>>> usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence. >>>>>>>>>>> This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created >>>>>>>>>>> nonfunctional copies in cell culture and found that 44 of them that >>>>>>>>>>> significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from >>>>>>>>>>> noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the >>>>>>>>>>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion. >>>>>>>>>>>
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have >>>>>>>>>> recently originated entirely de novo from noncoding sequences" >>>>>>>>>>
If the authors mean to say the *functions* are de novo, that would >>>>>>>>>> contradict Behe's claim that functional novelty appears rarely. >>>>>>>>>>
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional >>>>>>>>> regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding >>>>>>>>> DNA, but mutations had to happen to get it transcribed and for it to >>>>>>>>> encode the amino acid sequence of the microprotein. It needed a start >>>>>>>>> codon and a termination codon, and a protein sequence that fulfilled >>>>>>>>> some new function.
Ron Okimoto
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-) >>>>>>>
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
The place holder sequence would have to change over time while keeping >>>>>> enough of the sequence the same so that it could be determined that >>>>>> there was place holder sequence there at one time that changed into a >>>>>> functional gene.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell >>>>>> culture, the ID perps would claim that they were designed to fulfill the >>>>>> purpose that they now have. They were designed by an evolutionary >>>>>> process, but that doesn't seem to matter for ID perps like Behe. Behe >>>>>> understands that biological evolution is a fact of nature. He just >>>>>> thinks that the designer has something to do with getting the right >>>>>> mutations into the sequence at the right time to create the evolution >>>>>> that has been observed.
IIUC your description above severely understates Behe's expressed
disagreement about mutations. All of his books and lectures about ID >>>>> assert a common theme, that the "right" mutations are just too
improbable to have happened by unguided natural processes. That's why >>>>> he presumes a purposeful designer, to force the creation of those
"right" mutations that would not and could not have happened at the
right time and place and sequence. That's very different from your
description above, which implies that the "right" mutations appeared >>>>> just *as if* they were caused by unguided natural processes but *in
fact* God purposely made them appear that way. If that was Behe's
claim, he would have utterly no basis for claiming that unguided
natural processes are insufficient to explain the diversity (and
disparity) of life on Earth.
This seems to be just restating what I wrote. "Behe understands that
biological evolution is a fact of nature. He just thinks that the
designer has something to do with getting the right mutations into the >>>> sequence at the right time to create the evolution that has been observed."
There's a difference between claiming "right mutations" are too
improbable without a purposeful intelligent agent, and claiming that a
purposeful intelligent agent just happened to decide the way "right
mutations" would have happened all by themselves anyway. The latter
is just a version of shooting an arrow and then drawing a target
around whatever it hit, and would not support the claims and
conclusions Behe makes.
Behe is obviously claiming both.
Behe obviously can't claim both logically; one excludes the other.
His argument is that if his 3 neutral
mutations did occur in his IC systems that they would not have occurred
in a reasonable time without designer assistance. So he makes both
claims. If it is nearly impossible for something to have happened by
natural mechanisms, his designer must have done it.
The argument you describe above is circular. It *presumes* some
sequences are nearly impossible and therefore must have been by a
purposeful designer. In order for that line of reasoning to be
credible, it has to identify a basis for claiming a sequence which
Behe admits happened could not have happened by unguided natural
processes. Similarly, to allow that unguided natural processes caused
some de novo features, it has to identify a basis for claiming that
unguided natural processes caused *no* de novo features. Bald
asssertions and made-up statistics don't qualify as valid bases.
Behe really does
claim that his designer tweeks things as life has evolved on this
planet. Behe's designer takes genes that already exist and makes sure
that the right mutations occur at the right time to evolve the new
function. He acknowledges that research like Thornton's on the steroid
receptor genes is valid and that Thornton was able to recreate the
ancestral protein sequence and determine that 2 neutral mutations
occurred to create the new ligand binding capacity that created a whole
new family of steroid receptors. Behe even acknowledged that 2 neutral
mutations could have evolved by natural known mechanisms, he only
denigrated the finding by claiming that his designer could have done
better, and that his designer would be needed to put in 3 neutral
mutations to create a new function. No one has ever identified such an
example, but Behe really tries to denigrate Thornton's findings by
claiming that 2 neutral mutations are on the "edge of evolution" in
that, that is as far as natural mechanisms can be expected to go in
terms of the evolution of life on earth. Behe really is claiming that
his designer is involved in the tweeking to evolve things past the
boundary that he has created in his mind. It is still biological
evolution, but with designer assistance.
Just think about Behe's whale devolution and evolution by breaking
things stupidity. Behe really does claim that natural "Darwinian"
mechanisms can account for the whale evolution that we have figured out
so far. He calls it evolution by breaking things because a terrestrial
mammal that had evolved for a couple hundred million years adapting to
life on land and to make the transition back to the water. It is a
really stupid creationist argument because Behe is claiming that whales
could have evolved when the designer wasn't looking, and that it was
evolution so bad that his designer didn't have to be involved. Behe
claims that his designer was needed to do the really nifty things like
design his IC systems. The flagellum evolved over a billion years ago,
the blood clotting and adaptive immune systems evolved around half a
billion years ago. The aquatic ancestors of whales had these systems
before the tried to make a living on dry land, and whales took these IC
systems back into the water with them. Systems that they had inherited >>from their ancestors.
I allow the possibility that Behe makes both claims. My point here is
making both claims puts Behe logically arguing against himself. If he presumes a purposeful designer is required some times, he might as
well presume so all the time. Similarly, if he presumes unguided
natural processes are sufficient some times, he might as well presume
so all the time. He needs to pick his poison.
Behe thinks that his IC systems needed Designer help to get the right
mutations in the right place within the time that it took. He has
repeatedly claimed that one of his criteria is that it is impossible to >>>> get the needed mutations that he claims exists that created his systems >>>> in the time that was available. It is why he put up his "waiting time" >>>> argument claiming that populations of a given size would be unable to
create his two neutral mutations to produce a given function within some >>>> reasonable time frame. He just doesn't have any evidence that his type >>>> of evolution ever occurred in the populations that he claims that they >>>> would be unlikely to occur in. He knows that 2 neutral mutations would >>>> routinely occur to produce a given function (if it were possible) in the >>>> populations that evolved his IC systems because the population sizes
were likely greater than a trillion at any given time when the flagellum >>>> was evolving or blood clotting and the adaptive immune system, so he had >>>> to go with 3 neutral mutations to produce a function, but we have never >>>> identified any such thing ever occurring, and Behe pretty much refuses >>>> to look for them. The population limit applies to lineages like the ape >>>> lineage or the elephant lineage where the likely in the hundreds of
thousands to millions at most. We have never identified Behe's two
neutral mutations in such lineages, but Thornton did find 2 neutral
mutations involved in the change of ligand binding for steroid
receptors, but that evolution occurred before multicellular animals
evolved and the cell populations were likely large enough to have such a >>>> thing occur routinely. The limitation was likely if the rest of the
cellular functions were ready to take advantage of the mutations so that >>>> the new function could be selected for once the mutations had occurred. >>>>
Ron Okimoto
On Sat, 31 Dec 2022 02:35:41 -0800 (PST), Robert Carnegie <rja.ca...@excite.com> wrote:
On Friday, 30 December 2022 at 16:05:35 UTC, jillery wrote:
On Fri, 30 Dec 2022 06:45:54 -0800 (PST), Robert Carnegie
<rja.ca...@excite.com> wrote:
On Friday, 30 December 2022 at 07:45:35 UTC, jillery wrote:
On Thu, 29 Dec 2022 16:42:26 -0800 (PST), Robert Carnegie
<rja.ca...@excite.com> wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote:
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the >> >> >> sense that Behe means of being purposefully designed.
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote: >> >> >> >>
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from >> >> >> >>> noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the >> >> >> >>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have >> >> >> >> recently originated entirely de novo from noncoding sequences"
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely. >> >> >> >>
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional >> >> >> >regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Perhaps "we" aren't, but Behe and other cdesign proponentsists are.
Are they discussing real genes that were purposefully
designed? I'm presuming no and no. Genes are only
purposefully designed in a laboratory, and mostly not
even that, but by copying. I think copying, such as in
mRNA vaccines, doesn't amount to design.
As you should know, "they" use a different meaning of "purposefully
designed" than you and I do.
Do you mean they're lying? That, I do know.Since you asked, no. People can disagree without being deceptive
about it. There's a difference.
Should I really know what they mean, other than"should" in the sense they have been quoted regularly in T.O., and
that they mean to deceive?
other publications also mentioned in T.O. Your semi-regular posts
here suggest you read other's posts at least as often.
On 12/31/2022 10:42 AM, jillery wrote:
On Sat, 31 Dec 2022 07:56:17 -0600, RonO <rokimoto@cox.net> wrote:
On 12/31/2022 3:37 AM, jillery wrote:
On Fri, 30 Dec 2022 19:53:14 -0600, RonO <rokimoto@cox.net> wrote:
On 12/30/2022 6:40 AM, jillery wrote:
On Fri, 30 Dec 2022 04:56:39 -0600, RonO <rokimoto@cox.net> wrote: >>>>>>
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote: >>>>>>>>> On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>>
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the >>>>>>>>> sense that Behe means of being purposefully designed.
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>>>>
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created >>>>>>>>>>>> nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from >>>>>>>>>>>> noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the >>>>>>>>>>>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have >>>>>>>>>>> recently originated entirely de novo from noncoding sequences" >>>>>>>>>>>
If the authors mean to say the *functions* are de novo, that would >>>>>>>>>>> contradict Behe's claim that functional novelty appears rarely. >>>>>>>>>>>
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional >>>>>>>>>> regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to >>>>>>>>>> encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled >>>>>>>>>> some new function.
Ron Okimoto
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-) >>>>>>>>
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
The place holder sequence would have to change over time while keeping >>>>>>> enough of the sequence the same so that it could be determined that >>>>>>> there was place holder sequence there at one time that changed into a >>>>>>> functional gene.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell >>>>>>> culture, the ID perps would claim that they were designed to fulfill the
purpose that they now have. They were designed by an evolutionary >>>>>>> process, but that doesn't seem to matter for ID perps like Behe. Behe >>>>>>> understands that biological evolution is a fact of nature. He just >>>>>>> thinks that the designer has something to do with getting the right >>>>>>> mutations into the sequence at the right time to create the evolution >>>>>>> that has been observed.
IIUC your description above severely understates Behe's expressed
disagreement about mutations. All of his books and lectures about ID >>>>>> assert a common theme, that the "right" mutations are just too
improbable to have happened by unguided natural processes. That's why >>>>>> he presumes a purposeful designer, to force the creation of those
"right" mutations that would not and could not have happened at the >>>>>> right time and place and sequence. That's very different from your >>>>>> description above, which implies that the "right" mutations appeared >>>>>> just *as if* they were caused by unguided natural processes but *in >>>>>> fact* God purposely made them appear that way. If that was Behe's >>>>>> claim, he would have utterly no basis for claiming that unguided
natural processes are insufficient to explain the diversity (and
disparity) of life on Earth.
This seems to be just restating what I wrote. "Behe understands that >>>>> biological evolution is a fact of nature. He just thinks that the
designer has something to do with getting the right mutations into the >>>>> sequence at the right time to create the evolution that has been observed."
There's a difference between claiming "right mutations" are too
improbable without a purposeful intelligent agent, and claiming that a >>>> purposeful intelligent agent just happened to decide the way "right
mutations" would have happened all by themselves anyway. The latter
is just a version of shooting an arrow and then drawing a target
around whatever it hit, and would not support the claims and
conclusions Behe makes.
Behe is obviously claiming both.
Behe obviously can't claim both logically; one excludes the other.
His argument is that if his 3 neutral
mutations did occur in his IC systems that they would not have occurred
in a reasonable time without designer assistance. So he makes both
claims. If it is nearly impossible for something to have happened by
natural mechanisms, his designer must have done it.
The argument you describe above is circular. It *presumes* some
sequences are nearly impossible and therefore must have been by a
purposeful designer. In order for that line of reasoning to be
credible, it has to identify a basis for claiming a sequence which
Behe admits happened could not have happened by unguided natural
processes. Similarly, to allow that unguided natural processes caused
some de novo features, it has to identify a basis for claiming that
unguided natural processes caused *no* de novo features. Bald
asssertions and made-up statistics don't qualify as valid bases.
I never claimed that Behe's claims needed to be logically consistent nor >viable arguments. They are just what they are.
Behe really does
claim that his designer tweeks things as life has evolved on this
planet. Behe's designer takes genes that already exist and makes sure
that the right mutations occur at the right time to evolve the new
function. He acknowledges that research like Thornton's on the steroid
receptor genes is valid and that Thornton was able to recreate the
ancestral protein sequence and determine that 2 neutral mutations
occurred to create the new ligand binding capacity that created a whole
new family of steroid receptors. Behe even acknowledged that 2 neutral
mutations could have evolved by natural known mechanisms, he only
denigrated the finding by claiming that his designer could have done
better, and that his designer would be needed to put in 3 neutral
mutations to create a new function. No one has ever identified such an
example, but Behe really tries to denigrate Thornton's findings by
claiming that 2 neutral mutations are on the "edge of evolution" in
that, that is as far as natural mechanisms can be expected to go in
terms of the evolution of life on earth. Behe really is claiming that
his designer is involved in the tweeking to evolve things past the
boundary that he has created in his mind. It is still biological
evolution, but with designer assistance.
Just think about Behe's whale devolution and evolution by breaking
things stupidity. Behe really does claim that natural "Darwinian"
mechanisms can account for the whale evolution that we have figured out
so far. He calls it evolution by breaking things because a terrestrial
mammal that had evolved for a couple hundred million years adapting to
life on land and to make the transition back to the water. It is a
really stupid creationist argument because Behe is claiming that whales
could have evolved when the designer wasn't looking, and that it was
evolution so bad that his designer didn't have to be involved. Behe
claims that his designer was needed to do the really nifty things like
design his IC systems. The flagellum evolved over a billion years ago,
the blood clotting and adaptive immune systems evolved around half a
billion years ago. The aquatic ancestors of whales had these systems
before the tried to make a living on dry land, and whales took these IC
systems back into the water with them. Systems that they had inherited >>>from their ancestors.
I allow the possibility that Behe makes both claims. My point here is
making both claims puts Behe logically arguing against himself. If he
presumes a purposeful designer is required some times, he might as
well presume so all the time. Similarly, if he presumes unguided
natural processes are sufficient some times, he might as well presume
so all the time. He needs to pick his poison.
Like I just claimed Behe's junk arguments, don't have to be anything
more than the obfuscation and denial that they are meant to be. They
don't have to be logical, nor viable arguments. They are just what they >are.
Ron Okimoto
Behe thinks that his IC systems needed Designer help to get the right >>>>> mutations in the right place within the time that it took. He has
repeatedly claimed that one of his criteria is that it is impossible to >>>>> get the needed mutations that he claims exists that created his systems >>>>> in the time that was available. It is why he put up his "waiting time" >>>>> argument claiming that populations of a given size would be unable to >>>>> create his two neutral mutations to produce a given function within some >>>>> reasonable time frame. He just doesn't have any evidence that his type >>>>> of evolution ever occurred in the populations that he claims that they >>>>> would be unlikely to occur in. He knows that 2 neutral mutations would >>>>> routinely occur to produce a given function (if it were possible) in the >>>>> populations that evolved his IC systems because the population sizes >>>>> were likely greater than a trillion at any given time when the flagellum >>>>> was evolving or blood clotting and the adaptive immune system, so he had >>>>> to go with 3 neutral mutations to produce a function, but we have never >>>>> identified any such thing ever occurring, and Behe pretty much refuses >>>>> to look for them. The population limit applies to lineages like the ape >>>>> lineage or the elephant lineage where the likely in the hundreds of
thousands to millions at most. We have never identified Behe's two
neutral mutations in such lineages, but Thornton did find 2 neutral
mutations involved in the change of ligand binding for steroid
receptors, but that evolution occurred before multicellular animals
evolved and the cell populations were likely large enough to have such a >>>>> thing occur routinely. The limitation was likely if the rest of the >>>>> cellular functions were ready to take advantage of the mutations so that >>>>> the new function could be selected for once the mutations had occurred. >>>>>
Ron Okimoto
On Saturday, 31 December 2022 at 11:50:36 UTC, jillery wrote:
On Sat, 31 Dec 2022 02:35:41 -0800 (PST), Robert Carnegie
<rja.ca...@excite.com> wrote:
On Friday, 30 December 2022 at 16:05:35 UTC, jillery wrote:Since you asked, no. People can disagree without being deceptive
On Fri, 30 Dec 2022 06:45:54 -0800 (PST), Robert Carnegie
<rja.ca...@excite.com> wrote:
On Friday, 30 December 2022 at 07:45:35 UTC, jillery wrote:
On Thu, 29 Dec 2022 16:42:26 -0800 (PST), Robert CarnegieAre they discussing real genes that were purposefully
<rja.ca...@excite.com> wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote:
On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote: >> >> >> >>
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from
noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the
evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences" >> >> >> >> >>
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely. >> >> >> >> >>
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional >> >> >> >> >regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-)
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Perhaps "we" aren't, but Behe and other cdesign proponentsists are. >> >> >
designed? I'm presuming no and no. Genes are only
purposefully designed in a laboratory, and mostly not
even that, but by copying. I think copying, such as in
mRNA vaccines, doesn't amount to design.
As you should know, "they" use a different meaning of "purposefully
designed" than you and I do.
Do you mean they're lying? That, I do know.
about it. There's a difference.
Should I really know what they mean, other than"should" in the sense they have been quoted regularly in T.O., and
that they mean to deceive?
other publications also mentioned in T.O. Your semi-regular posts
here suggest you read other's posts at least as often.
Real scientists do fool around with words - such as
when they decided that "oxidation" doesn't have to mean
the formation of an oxide, any more - but if words are
used without regard to an accepted meaning in context,
that's simply dishonest. Or even if it isn't, my opinion
is that Behe & co. are committing adultery. Since apparently
I can call it that, if I want to. I can call it whatever I like.
They are adulterating language, for people to be
purposefully deceived.
[ … ]
Real scientists do fool around with words - such as
when they decided that "oxidation" doesn't have to mean
the formation of an oxide, any more
- but if words are
used without regard to an accepted meaning in context,
that's simply dishonest. Or even if it isn't, my opinion
is that Behe & co. are committing adultery. Since apparently
I can call it that, if I want to. I can call it whatever I like.
They are adulterating language, for people to be
purposefully deceived.
On Sat, 31 Dec 2022 11:23:35 -0600, RonO <rokimoto@cox.net> wrote:
On 12/31/2022 10:42 AM, jillery wrote:
On Sat, 31 Dec 2022 07:56:17 -0600, RonO <rokimoto@cox.net> wrote:
On 12/31/2022 3:37 AM, jillery wrote:
On Fri, 30 Dec 2022 19:53:14 -0600, RonO <rokimoto@cox.net> wrote:
On 12/30/2022 6:40 AM, jillery wrote:
On Fri, 30 Dec 2022 04:56:39 -0600, RonO <rokimoto@cox.net> wrote: >>>>>>>
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote: >>>>>>>>>> On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>>>
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the >>>>>>>>>> sense that Behe means of being purposefully designed.
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>>>>>
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from >>>>>>>>>>>>> noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the >>>>>>>>>>>>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have >>>>>>>>>>>> recently originated entirely de novo from noncoding sequences" >>>>>>>>>>>>
If the authors mean to say the *functions* are de novo, that would >>>>>>>>>>>> contradict Behe's claim that functional novelty appears rarely. >>>>>>>>>>>>
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional >>>>>>>>>>> regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
On the contrary, maybe the noncoding DNA was created by God
as a placeholder for the new gene that He would create later. :-) >>>>>>>>>
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
The place holder sequence would have to change over time while keeping >>>>>>>> enough of the sequence the same so that it could be determined that >>>>>>>> there was place holder sequence there at one time that changed into a >>>>>>>> functional gene.
But in fact, while I don't understand most of this matter,
I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell >>>>>>>> culture, the ID perps would claim that they were designed to fulfill the
purpose that they now have. They were designed by an evolutionary >>>>>>>> process, but that doesn't seem to matter for ID perps like Behe. Behe >>>>>>>> understands that biological evolution is a fact of nature. He just >>>>>>>> thinks that the designer has something to do with getting the right >>>>>>>> mutations into the sequence at the right time to create the evolution >>>>>>>> that has been observed.
IIUC your description above severely understates Behe's expressed >>>>>>> disagreement about mutations. All of his books and lectures about ID >>>>>>> assert a common theme, that the "right" mutations are just too
improbable to have happened by unguided natural processes. That's why >>>>>>> he presumes a purposeful designer, to force the creation of those >>>>>>> "right" mutations that would not and could not have happened at the >>>>>>> right time and place and sequence. That's very different from your >>>>>>> description above, which implies that the "right" mutations appeared >>>>>>> just *as if* they were caused by unguided natural processes but *in >>>>>>> fact* God purposely made them appear that way. If that was Behe's >>>>>>> claim, he would have utterly no basis for claiming that unguided >>>>>>> natural processes are insufficient to explain the diversity (and >>>>>>> disparity) of life on Earth.
This seems to be just restating what I wrote. "Behe understands that >>>>>> biological evolution is a fact of nature. He just thinks that the >>>>>> designer has something to do with getting the right mutations into the >>>>>> sequence at the right time to create the evolution that has been observed."
There's a difference between claiming "right mutations" are too
improbable without a purposeful intelligent agent, and claiming that a >>>>> purposeful intelligent agent just happened to decide the way "right
mutations" would have happened all by themselves anyway. The latter >>>>> is just a version of shooting an arrow and then drawing a target
around whatever it hit, and would not support the claims and
conclusions Behe makes.
Behe is obviously claiming both.
Behe obviously can't claim both logically; one excludes the other.
His argument is that if his 3 neutral
mutations did occur in his IC systems that they would not have occurred >>>> in a reasonable time without designer assistance. So he makes both
claims. If it is nearly impossible for something to have happened by
natural mechanisms, his designer must have done it.
The argument you describe above is circular. It *presumes* some
sequences are nearly impossible and therefore must have been by a
purposeful designer. In order for that line of reasoning to be
credible, it has to identify a basis for claiming a sequence which
Behe admits happened could not have happened by unguided natural
processes. Similarly, to allow that unguided natural processes caused
some de novo features, it has to identify a basis for claiming that
unguided natural processes caused *no* de novo features. Bald
asssertions and made-up statistics don't qualify as valid bases.
I never claimed that Behe's claims needed to be logically consistent nor
viable arguments. They are just what they are.
And I never claimed you claimed... My focus is on what Behe says.
Behe really does
claim that his designer tweeks things as life has evolved on this
planet. Behe's designer takes genes that already exist and makes sure >>>> that the right mutations occur at the right time to evolve the new
function. He acknowledges that research like Thornton's on the steroid >>>> receptor genes is valid and that Thornton was able to recreate the
ancestral protein sequence and determine that 2 neutral mutations
occurred to create the new ligand binding capacity that created a whole >>>> new family of steroid receptors. Behe even acknowledged that 2 neutral >>>> mutations could have evolved by natural known mechanisms, he only
denigrated the finding by claiming that his designer could have done
better, and that his designer would be needed to put in 3 neutral
mutations to create a new function. No one has ever identified such an >>>> example, but Behe really tries to denigrate Thornton's findings by
claiming that 2 neutral mutations are on the "edge of evolution" in
that, that is as far as natural mechanisms can be expected to go in
terms of the evolution of life on earth. Behe really is claiming that >>>> his designer is involved in the tweeking to evolve things past the
boundary that he has created in his mind. It is still biological
evolution, but with designer assistance.
Just think about Behe's whale devolution and evolution by breaking
things stupidity. Behe really does claim that natural "Darwinian"
mechanisms can account for the whale evolution that we have figured out >>>> so far. He calls it evolution by breaking things because a terrestrial >>>> mammal that had evolved for a couple hundred million years adapting to >>>> life on land and to make the transition back to the water. It is a
really stupid creationist argument because Behe is claiming that whales >>>> could have evolved when the designer wasn't looking, and that it was
evolution so bad that his designer didn't have to be involved. Behe
claims that his designer was needed to do the really nifty things like >>>> design his IC systems. The flagellum evolved over a billion years ago, >>>> the blood clotting and adaptive immune systems evolved around half a
billion years ago. The aquatic ancestors of whales had these systems
before the tried to make a living on dry land, and whales took these IC >>>> systems back into the water with them. Systems that they had inherited >>> >from their ancestors.
I allow the possibility that Behe makes both claims. My point here is
making both claims puts Behe logically arguing against himself. If he
presumes a purposeful designer is required some times, he might as
well presume so all the time. Similarly, if he presumes unguided
natural processes are sufficient some times, he might as well presume
so all the time. He needs to pick his poison.
Like I just claimed Behe's junk arguments, don't have to be anything
more than the obfuscation and denial that they are meant to be. They
don't have to be logical, nor viable arguments. They are just what they
are.
Ron Okimoto
Behe thinks that his IC systems needed Designer help to get the right >>>>>> mutations in the right place within the time that it took. He has >>>>>> repeatedly claimed that one of his criteria is that it is impossible to >>>>>> get the needed mutations that he claims exists that created his systems >>>>>> in the time that was available. It is why he put up his "waiting time" >>>>>> argument claiming that populations of a given size would be unable to >>>>>> create his two neutral mutations to produce a given function within some >>>>>> reasonable time frame. He just doesn't have any evidence that his type >>>>>> of evolution ever occurred in the populations that he claims that they >>>>>> would be unlikely to occur in. He knows that 2 neutral mutations would >>>>>> routinely occur to produce a given function (if it were possible) in the >>>>>> populations that evolved his IC systems because the population sizes >>>>>> were likely greater than a trillion at any given time when the flagellum >>>>>> was evolving or blood clotting and the adaptive immune system, so he had >>>>>> to go with 3 neutral mutations to produce a function, but we have never >>>>>> identified any such thing ever occurring, and Behe pretty much refuses >>>>>> to look for them. The population limit applies to lineages like the ape >>>>>> lineage or the elephant lineage where the likely in the hundreds of >>>>>> thousands to millions at most. We have never identified Behe's two >>>>>> neutral mutations in such lineages, but Thornton did find 2 neutral >>>>>> mutations involved in the change of ligand binding for steroid
receptors, but that evolution occurred before multicellular animals >>>>>> evolved and the cell populations were likely large enough to have such a >>>>>> thing occur routinely. The limitation was likely if the rest of the >>>>>> cellular functions were ready to take advantage of the mutations so that >>>>>> the new function could be selected for once the mutations had occurred. >>>>>>
Ron Okimoto
On 2023-01-01 01:47:30 +0000, Robert Carnegie said:
[ … ]
Real scientists do fool around with words - such asYou say that as if it were something new, but "oxidation" was alrady
when they decided that "oxidation" doesn't have to mean
the formation of an oxide, any more
used in a broad sense when I was studying chemistry in the 1960s. I
didn't like it then and I don't like it now, but they didn't consult me.
- but if words are
used without regard to an accepted meaning in context,
that's simply dishonest. Or even if it isn't, my opinion
is that Behe & co. are committing adultery. Since apparently
I can call it that, if I want to. I can call it whatever I like.
They are adulterating language, for people to be
purposefully deceived.
On 12/31/2022 7:56 PM, jillery wrote:
On Sat, 31 Dec 2022 11:23:35 -0600, RonO <rokimoto@cox.net> wrote:
On 12/31/2022 10:42 AM, jillery wrote:
On Sat, 31 Dec 2022 07:56:17 -0600, RonO <rokimoto@cox.net> wrote:
On 12/31/2022 3:37 AM, jillery wrote:
On Fri, 30 Dec 2022 19:53:14 -0600, RonO <rokimoto@cox.net> wrote: >>>>>>
On 12/30/2022 6:40 AM, jillery wrote:
On Fri, 30 Dec 2022 04:56:39 -0600, RonO <rokimoto@cox.net> wrote: >>>>>>>>
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote: >>>>>>>>>>> On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>>>>
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the >>>>>>>>>>> sense that Behe means of being purposefully designed.
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>>>>>>
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from >>>>>>>>>>>>>> noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the >>>>>>>>>>>>>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have >>>>>>>>>>>>> recently originated entirely de novo from noncoding sequences" >>>>>>>>>>>>>
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely. >>>>>>>>>>>>>
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional >>>>>>>>>>>> regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
On the contrary, maybe the noncoding DNA was created by God >>>>>>>>>> as a placeholder for the new gene that He would create later. :-) >>>>>>>>>>
Maybe God doesn't have to do this, but that does not mean
that He wouldn't.
The place holder sequence would have to change over time while keeping
enough of the sequence the same so that it could be determined that >>>>>>>>> there was place holder sequence there at one time that changed into a >>>>>>>>> functional gene.
But in fact, while I don't understand most of this matter, >>>>>>>>>> I am confident that we aren't discussing a gene that was
purposefully designed.
Since these new genes were determined to have fitness effects in cell >>>>>>>>> culture, the ID perps would claim that they were designed to fulfill the
purpose that they now have. They were designed by an evolutionary >>>>>>>>> process, but that doesn't seem to matter for ID perps like Behe. Behe
understands that biological evolution is a fact of nature. He just >>>>>>>>> thinks that the designer has something to do with getting the right >>>>>>>>> mutations into the sequence at the right time to create the evolution >>>>>>>>> that has been observed.
IIUC your description above severely understates Behe's expressed >>>>>>>> disagreement about mutations. All of his books and lectures about ID >>>>>>>> assert a common theme, that the "right" mutations are just too >>>>>>>> improbable to have happened by unguided natural processes. That's why >>>>>>>> he presumes a purposeful designer, to force the creation of those >>>>>>>> "right" mutations that would not and could not have happened at the >>>>>>>> right time and place and sequence. That's very different from your >>>>>>>> description above, which implies that the "right" mutations appeared >>>>>>>> just *as if* they were caused by unguided natural processes but *in >>>>>>>> fact* God purposely made them appear that way. If that was Behe's >>>>>>>> claim, he would have utterly no basis for claiming that unguided >>>>>>>> natural processes are insufficient to explain the diversity (and >>>>>>>> disparity) of life on Earth.
This seems to be just restating what I wrote. "Behe understands that >>>>>>> biological evolution is a fact of nature. He just thinks that the >>>>>>> designer has something to do with getting the right mutations into the >>>>>>> sequence at the right time to create the evolution that has been observed."
There's a difference between claiming "right mutations" are too
improbable without a purposeful intelligent agent, and claiming that a >>>>>> purposeful intelligent agent just happened to decide the way "right >>>>>> mutations" would have happened all by themselves anyway. The latter >>>>>> is just a version of shooting an arrow and then drawing a target
around whatever it hit, and would not support the claims and
conclusions Behe makes.
Behe is obviously claiming both.
Behe obviously can't claim both logically; one excludes the other.
His argument is that if his 3 neutral
mutations did occur in his IC systems that they would not have occurred >>>>> in a reasonable time without designer assistance. So he makes both
claims. If it is nearly impossible for something to have happened by >>>>> natural mechanisms, his designer must have done it.
The argument you describe above is circular. It *presumes* some
sequences are nearly impossible and therefore must have been by a
purposeful designer. In order for that line of reasoning to be
credible, it has to identify a basis for claiming a sequence which
Behe admits happened could not have happened by unguided natural
processes. Similarly, to allow that unguided natural processes caused >>>> some de novo features, it has to identify a basis for claiming that
unguided natural processes caused *no* de novo features. Bald
asssertions and made-up statistics don't qualify as valid bases.
I never claimed that Behe's claims needed to be logically consistent nor >>> viable arguments. They are just what they are.
And I never claimed you claimed... My focus is on what Behe says.
The other ID perps have called Behe the super hero of the ID scam, but
most of the creationist support for the ID scam is anti-evolution and
YEC to boot, and Behe has consistently told the IDiot creationist rubes
that biological evolution is a fact of nature, and claims that his
designer diddle farted around with his IC systems over a billion years
ago for the bacterial flagellum, and the steroid receptor neutral
mutations that Behe claimed were "on the edge of evolution" (something
that Darwinian mechanisms could do) occurred before the Cambrian
explosion and the evolution of most of the multicellular phyla. Behe >admitted that 2 neutral mutations could be accomplished by Darwinian >mechanisms, but he denigrated the evolution, and claimed that his
designer was needed to put in 3 neutral mutations. It is just sad that
no one has identified where 3 neutral mutations needed to occur in any >system in order to create a new function.
Behe has been the IDiot savant that the ID perps try to hide in the
closet, but they keep bringing out to play his harmonica every once in a >while.
He has been more of a Stupor hero than a super hero for the ID scam.
Ask Glenn what he thinks about Behe's evolutionary views. Sewell
dropped IC out of the Top Six best evidences for the ID scam.
Ron Okimoto
Behe really does
claim that his designer tweeks things as life has evolved on this
planet. Behe's designer takes genes that already exist and makes sure >>>>> that the right mutations occur at the right time to evolve the new
function. He acknowledges that research like Thornton's on the steroid >>>>> receptor genes is valid and that Thornton was able to recreate the
ancestral protein sequence and determine that 2 neutral mutations
occurred to create the new ligand binding capacity that created a whole >>>>> new family of steroid receptors. Behe even acknowledged that 2 neutral >>>>> mutations could have evolved by natural known mechanisms, he only
denigrated the finding by claiming that his designer could have done >>>>> better, and that his designer would be needed to put in 3 neutral
mutations to create a new function. No one has ever identified such an >>>>> example, but Behe really tries to denigrate Thornton's findings by
claiming that 2 neutral mutations are on the "edge of evolution" in
that, that is as far as natural mechanisms can be expected to go in
terms of the evolution of life on earth. Behe really is claiming that >>>>> his designer is involved in the tweeking to evolve things past the
boundary that he has created in his mind. It is still biological
evolution, but with designer assistance.
Just think about Behe's whale devolution and evolution by breaking
things stupidity. Behe really does claim that natural "Darwinian"
mechanisms can account for the whale evolution that we have figured out >>>>> so far. He calls it evolution by breaking things because a terrestrial >>>>> mammal that had evolved for a couple hundred million years adapting to >>>>> life on land and to make the transition back to the water. It is a
really stupid creationist argument because Behe is claiming that whales >>>>> could have evolved when the designer wasn't looking, and that it was >>>>> evolution so bad that his designer didn't have to be involved. Behe >>>>> claims that his designer was needed to do the really nifty things like >>>>> design his IC systems. The flagellum evolved over a billion years ago, >>>>> the blood clotting and adaptive immune systems evolved around half a >>>>> billion years ago. The aquatic ancestors of whales had these systems >>>>> before the tried to make a living on dry land, and whales took these IC >>>>> systems back into the water with them. Systems that they had inherited >>>> >from their ancestors.
I allow the possibility that Behe makes both claims. My point here is >>>> making both claims puts Behe logically arguing against himself. If he >>>> presumes a purposeful designer is required some times, he might as
well presume so all the time. Similarly, if he presumes unguided
natural processes are sufficient some times, he might as well presume
so all the time. He needs to pick his poison.
Like I just claimed Behe's junk arguments, don't have to be anything
more than the obfuscation and denial that they are meant to be. They
don't have to be logical, nor viable arguments. They are just what they >>> are.
Ron Okimoto
Behe thinks that his IC systems needed Designer help to get the right >>>>>>> mutations in the right place within the time that it took. He has >>>>>>> repeatedly claimed that one of his criteria is that it is impossible to >>>>>>> get the needed mutations that he claims exists that created his systems >>>>>>> in the time that was available. It is why he put up his "waiting time" >>>>>>> argument claiming that populations of a given size would be unable to >>>>>>> create his two neutral mutations to produce a given function within some
reasonable time frame. He just doesn't have any evidence that his type >>>>>>> of evolution ever occurred in the populations that he claims that they >>>>>>> would be unlikely to occur in. He knows that 2 neutral mutations would >>>>>>> routinely occur to produce a given function (if it were possible) in the
populations that evolved his IC systems because the population sizes >>>>>>> were likely greater than a trillion at any given time when the flagellum
was evolving or blood clotting and the adaptive immune system, so he had
to go with 3 neutral mutations to produce a function, but we have never >>>>>>> identified any such thing ever occurring, and Behe pretty much refuses >>>>>>> to look for them. The population limit applies to lineages like the ape
lineage or the elephant lineage where the likely in the hundreds of >>>>>>> thousands to millions at most. We have never identified Behe's two >>>>>>> neutral mutations in such lineages, but Thornton did find 2 neutral >>>>>>> mutations involved in the change of ligand binding for steroid
receptors, but that evolution occurred before multicellular animals >>>>>>> evolved and the cell populations were likely large enough to have such a
thing occur routinely. The limitation was likely if the rest of the >>>>>>> cellular functions were ready to take advantage of the mutations so that
the new function could be selected for once the mutations had occurred. >>>>>>>
Ron Okimoto
On Sun, 1 Jan 2023 06:50:05 -0600, RonO <rokimoto@cox.net> wrote:
On 12/31/2022 7:56 PM, jillery wrote:
On Sat, 31 Dec 2022 11:23:35 -0600, RonO <rokimoto@cox.net> wrote:
On 12/31/2022 10:42 AM, jillery wrote:
On Sat, 31 Dec 2022 07:56:17 -0600, RonO <rokimoto@cox.net> wrote:
On 12/31/2022 3:37 AM, jillery wrote:
On Fri, 30 Dec 2022 19:53:14 -0600, RonO <rokimoto@cox.net> wrote: >>>>>>>
On 12/30/2022 6:40 AM, jillery wrote:
On Fri, 30 Dec 2022 04:56:39 -0600, RonO <rokimoto@cox.net> wrote: >>>>>>>>>
On 12/29/2022 6:42 PM, Robert Carnegie wrote:
On Wednesday, 28 December 2022 at 04:25:33 UTC, jillery wrote: >>>>>>>>>>>> On Tue, 27 Dec 2022 17:06:06 -0600, RonO <roki...@cox.net> wrote: >>>>>>>>>>>>
On 12/27/2022 1:14 AM, jillery wrote:OK, that says to me the new gene isn't technically "de novo" in the
On Mon, 26 Dec 2022 07:14:52 -0600, RonO <roki...@cox.net> wrote:
https://pubmed.ncbi.nlm.nih.gov/36543139/
You can get to a free copy of the paper by going to the pubmed link and
clicking on the DOI.
This is a paper that looked at short open reading frames. These are
usually missed in most functional analyses because we often put some
arbitrary length of protein coding sequence to remove noise due to open
reading frames (ORF) that just happen by chance in random sequence.
This paper tracked down 144 of these short ORF genes that they could
determine had an evolutionary history (conserved from ancestral de novo
creation of the gene). They did knockout gene analysis and created
nonfunctional copies in cell culture and found that 44 of them that
significantly affected the cells in cell culture and had a measurable
fitness effect.
19 short ORF with measurable fitness effects had an origin within the
last 43 million years of primate evolution. 2 of the short ORF genes
with measurable fitness effects were found to have evolved from >>>>>>>>>>>>>>> noncoding sequence since the human lineage separated from chimps. They
think that such new genes might have an important effect in the >>>>>>>>>>>>>>> evolution of us and other species.
They discuss the limitations of their analysis in their discussion.
Behe should likely be looking for his IC mutations in these new genes
that had a measurable fitness effect.
Ron Okimoto
I am confused by the following from the abstract:
"it is plausible that some of these functional microproteins have
recently originated entirely de novo from noncoding sequences" >>>>>>>>>>>>>>
If the authors mean to say the *functions* are de novo, that would
contradict Behe's claim that functional novelty appears rarely. >>>>>>>>>>>>>>
OTOH if the authors mean to say the genes themselves are de novo, that
would contradict the authors claim that they tracked the origins back
to some noncoding sequence.
The paper just give evidence that the new coding genes evolved de novo
from non coding sequence. The open reading frame evolved to produce the
micro protein, and the sequence had to evolve the transcriptional >>>>>>>>>>>>> regulatory sequences needed to transcribe the gene and get it translated
by the ribosomes. The sequence existed in some ancestor as non coding
DNA, but mutations had to happen to get it transcribed and for it to
encode the amino acid sequence of the microprotein. It needed a start
codon and a termination codon, and a protein sequence that fulfilled
some new function.
Ron Okimoto
sense that Behe means of being purposefully designed.
On the contrary, maybe the noncoding DNA was created by God >>>>>>>>>>> as a placeholder for the new gene that He would create later. :-) >>>>>>>>>>>
Maybe God doesn't have to do this, but that does not mean >>>>>>>>>>> that He wouldn't.
The place holder sequence would have to change over time while keeping
enough of the sequence the same so that it could be determined that >>>>>>>>>> there was place holder sequence there at one time that changed into a
functional gene.
But in fact, while I don't understand most of this matter, >>>>>>>>>>> I am confident that we aren't discussing a gene that was >>>>>>>>>>> purposefully designed.
Since these new genes were determined to have fitness effects in cell
culture, the ID perps would claim that they were designed to fulfill the
purpose that they now have. They were designed by an evolutionary >>>>>>>>>> process, but that doesn't seem to matter for ID perps like Behe. Behe
understands that biological evolution is a fact of nature. He just >>>>>>>>>> thinks that the designer has something to do with getting the right >>>>>>>>>> mutations into the sequence at the right time to create the evolution
that has been observed.
IIUC your description above severely understates Behe's expressed >>>>>>>>> disagreement about mutations. All of his books and lectures about ID >>>>>>>>> assert a common theme, that the "right" mutations are just too >>>>>>>>> improbable to have happened by unguided natural processes. That's why
he presumes a purposeful designer, to force the creation of those >>>>>>>>> "right" mutations that would not and could not have happened at the >>>>>>>>> right time and place and sequence. That's very different from your >>>>>>>>> description above, which implies that the "right" mutations appeared >>>>>>>>> just *as if* they were caused by unguided natural processes but *in >>>>>>>>> fact* God purposely made them appear that way. If that was Behe's >>>>>>>>> claim, he would have utterly no basis for claiming that unguided >>>>>>>>> natural processes are insufficient to explain the diversity (and >>>>>>>>> disparity) of life on Earth.
This seems to be just restating what I wrote. "Behe understands that >>>>>>>> biological evolution is a fact of nature. He just thinks that the >>>>>>>> designer has something to do with getting the right mutations into the >>>>>>>> sequence at the right time to create the evolution that has been observed."
There's a difference between claiming "right mutations" are too
improbable without a purposeful intelligent agent, and claiming that a >>>>>>> purposeful intelligent agent just happened to decide the way "right >>>>>>> mutations" would have happened all by themselves anyway. The latter >>>>>>> is just a version of shooting an arrow and then drawing a target >>>>>>> around whatever it hit, and would not support the claims and
conclusions Behe makes.
Behe is obviously claiming both.
Behe obviously can't claim both logically; one excludes the other.
His argument is that if his 3 neutral
mutations did occur in his IC systems that they would not have occurred >>>>>> in a reasonable time without designer assistance. So he makes both >>>>>> claims. If it is nearly impossible for something to have happened by >>>>>> natural mechanisms, his designer must have done it.
The argument you describe above is circular. It *presumes* some
sequences are nearly impossible and therefore must have been by a
purposeful designer. In order for that line of reasoning to be
credible, it has to identify a basis for claiming a sequence which
Behe admits happened could not have happened by unguided natural
processes. Similarly, to allow that unguided natural processes caused >>>>> some de novo features, it has to identify a basis for claiming that
unguided natural processes caused *no* de novo features. Bald
asssertions and made-up statistics don't qualify as valid bases.
I never claimed that Behe's claims needed to be logically consistent nor >>>> viable arguments. They are just what they are.
And I never claimed you claimed... My focus is on what Behe says.
The other ID perps have called Behe the super hero of the ID scam, but
most of the creationist support for the ID scam is anti-evolution and
YEC to boot, and Behe has consistently told the IDiot creationist rubes
that biological evolution is a fact of nature, and claims that his
designer diddle farted around with his IC systems over a billion years
ago for the bacterial flagellum, and the steroid receptor neutral
mutations that Behe claimed were "on the edge of evolution" (something
that Darwinian mechanisms could do) occurred before the Cambrian
explosion and the evolution of most of the multicellular phyla. Behe
admitted that 2 neutral mutations could be accomplished by Darwinian
mechanisms, but he denigrated the evolution, and claimed that his
designer was needed to put in 3 neutral mutations. It is just sad that
no one has identified where 3 neutral mutations needed to occur in any
system in order to create a new function.
Behe has been the IDiot savant that the ID perps try to hide in the
closet, but they keep bringing out to play his harmonica every once in a
while.
He has been more of a Stupor hero than a super hero for the ID scam.
Ask Glenn what he thinks about Behe's evolutionary views. Sewell
dropped IC out of the Top Six best evidences for the ID scam.
Ron Okimoto
You and I both agree that Behe's claims are illogical and incoherent.
Based on that, ISTM it's impossible to discern what he actually means
by what he actually says.
Behe really does
claim that his designer tweeks things as life has evolved on this
planet. Behe's designer takes genes that already exist and makes sure >>>>>> that the right mutations occur at the right time to evolve the new >>>>>> function. He acknowledges that research like Thornton's on the steroid >>>>>> receptor genes is valid and that Thornton was able to recreate the >>>>>> ancestral protein sequence and determine that 2 neutral mutations
occurred to create the new ligand binding capacity that created a whole >>>>>> new family of steroid receptors. Behe even acknowledged that 2 neutral >>>>>> mutations could have evolved by natural known mechanisms, he only
denigrated the finding by claiming that his designer could have done >>>>>> better, and that his designer would be needed to put in 3 neutral
mutations to create a new function. No one has ever identified such an >>>>>> example, but Behe really tries to denigrate Thornton's findings by >>>>>> claiming that 2 neutral mutations are on the "edge of evolution" in >>>>>> that, that is as far as natural mechanisms can be expected to go in >>>>>> terms of the evolution of life on earth. Behe really is claiming that >>>>>> his designer is involved in the tweeking to evolve things past the >>>>>> boundary that he has created in his mind. It is still biological
evolution, but with designer assistance.
Just think about Behe's whale devolution and evolution by breaking >>>>>> things stupidity. Behe really does claim that natural "Darwinian" >>>>>> mechanisms can account for the whale evolution that we have figured out >>>>>> so far. He calls it evolution by breaking things because a terrestrial >>>>>> mammal that had evolved for a couple hundred million years adapting to >>>>>> life on land and to make the transition back to the water. It is a >>>>>> really stupid creationist argument because Behe is claiming that whales >>>>>> could have evolved when the designer wasn't looking, and that it was >>>>>> evolution so bad that his designer didn't have to be involved. Behe >>>>>> claims that his designer was needed to do the really nifty things like >>>>>> design his IC systems. The flagellum evolved over a billion years ago, >>>>>> the blood clotting and adaptive immune systems evolved around half a >>>>>> billion years ago. The aquatic ancestors of whales had these systems >>>>>> before the tried to make a living on dry land, and whales took these IC >>>>>> systems back into the water with them. Systems that they had inherited >>>>> >from their ancestors.
I allow the possibility that Behe makes both claims. My point here is >>>>> making both claims puts Behe logically arguing against himself. If he >>>>> presumes a purposeful designer is required some times, he might as
well presume so all the time. Similarly, if he presumes unguided
natural processes are sufficient some times, he might as well presume >>>>> so all the time. He needs to pick his poison.
Like I just claimed Behe's junk arguments, don't have to be anything
more than the obfuscation and denial that they are meant to be. They
don't have to be logical, nor viable arguments. They are just what they >>>> are.
Ron Okimoto
Behe thinks that his IC systems needed Designer help to get the right >>>>>>>> mutations in the right place within the time that it took. He has >>>>>>>> repeatedly claimed that one of his criteria is that it is impossible to
get the needed mutations that he claims exists that created his systems
in the time that was available. It is why he put up his "waiting time"
argument claiming that populations of a given size would be unable to >>>>>>>> create his two neutral mutations to produce a given function within some
reasonable time frame. He just doesn't have any evidence that his type
of evolution ever occurred in the populations that he claims that they >>>>>>>> would be unlikely to occur in. He knows that 2 neutral mutations would >>>>>>>> routinely occur to produce a given function (if it were possible) in the
populations that evolved his IC systems because the population sizes >>>>>>>> were likely greater than a trillion at any given time when the flagellum
was evolving or blood clotting and the adaptive immune system, so he had
to go with 3 neutral mutations to produce a function, but we have never
identified any such thing ever occurring, and Behe pretty much refuses >>>>>>>> to look for them. The population limit applies to lineages like the ape
lineage or the elephant lineage where the likely in the hundreds of >>>>>>>> thousands to millions at most. We have never identified Behe's two >>>>>>>> neutral mutations in such lineages, but Thornton did find 2 neutral >>>>>>>> mutations involved in the change of ligand binding for steroid >>>>>>>> receptors, but that evolution occurred before multicellular animals >>>>>>>> evolved and the cell populations were likely large enough to have such a
thing occur routinely. The limitation was likely if the rest of the >>>>>>>> cellular functions were ready to take advantage of the mutations so that
the new function could be selected for once the mutations had occurred.
Ron Okimoto
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