This article beautifully explains "how" hominoids c 25 Ma lost the tail.
The "why" is easier: they became bipedal in flooded/mangrove forests: wading upright + climbing arms overhead, google our TREE paper "Aquarboreal Ancestors".


The genetic basis of tail-loss evolution in humans and apes
Bo Xia cs 20121
https://doi.org/10.1101/2021.09.14.460388
The loss of the tail is one of the main anatomical evolutionary changes to have occurred along the lineage leading to humans & the “anthropomorphous apes”.
This morphological re-programming in the ancestral hominoids has been long considered to have accommodated a characteristic style of locomotion, and contributed to the evolution of bipedalism in humans.
Yet, the precise genetic mechanism that facilitated tail-loss evolution in hominoids remains unknown.
Primate genome sequencing projects have made possible the identification of causal links between genotypic & phenotypic changes, and enable the search for hominoid-specific genetic elements controlling tail development.
Here we present evidence that tail-loss evolution was mediated by the insertion of an individual Alu-element into the genome of the hominoid ancestor.
We demonstrate:
this Alu-element (inserted into an intron of the TBXT gene, also called T or Brachyury) pairs with a neighboring ancestral Alu-element encoded in the reverse genomic orientation, and leads to a hominoid-specific alternative splicing event.
To study the effect of this splicing event, we generated a mouse model that mimics the expression of human TBXT products by expressing both full-length & exon-skipped iso-forms of the mouse TBXT ortholog.
We found:
mice with this genotype exhibit the complete absence of a tail or a shortened tail, supporting the notion that the exon-skipped transcript is sufficient to induce a tail-loss phenotype, albeit with incomplete penetrance.
We further noted:
mice homozygous for the exon-skipped isoforms exhibited embryonic spinal cord malformations, resembling a neural tube defect, which affects ∼1/1000 human neonates.
We propose:
- selection for the loss of the tail along the hominoid lineage was ass.x an adaptive cost of potential neural tube defects,
- this ancient evolutionary trade-off may thus continue to affect human health today.

_______

‘Jumping gene’ may have erased tails in humans and other apes
— and boosted our risk of birth defects 21.9.21

Adding mobile DNA sequence to developmental gene short-circuits tail development in mice

Mammals from mice to monkeys have tails, but humans & great apes lack them. Now, researchers may have unearthed a simple genetic change that led to our abbreviated back end: an itinerant piece of DNA that leapt into a new chromosomal home, and changed
how great apes make a key developmental protein.
The finding also suggests the genetic shift came with a less visible & more dangerous effect: a higher risk of birth defects, involving the developing spinal cord.
Hopi Hoekstra (evol.biol.Harvard Univ.):
The work not only addresses an “inherently interesting question about what makes us human, but also provides new insights into how such evolutionary changes can occur. It’s beautiful work.”
Bo Xia (grad.student genome evolution NYU Grossman Sch.Medicine) wondered as a child why people didn’t have tails,
a tail-bone injury a few years ago renewed his curiosity.
A wealth of primate genomes has been sequenced in recent years, so he started to search for any ape-specific changes in genes known to play a role in tail development.
In a gene called TBXT, he found a strong suspect, a short DNA-insertion called an Alu element, present in all great apes, but missing in other primates.
Alu-sequences can move around the genome, and are sometimes called jumping genes or transposable elements.
Possibly remnants of ancient viruses, they’re common in the human genome, making up c 10 % of our DNA.
Sometimes an Alu-insertion interrupts a gene, and prevents its protein production,
in other cases, the elements have more complex effects, changing where or how a protein is expressed.
Pascal Gagneux (evol.biol.Univ.Calif. San Diego):
This makes them a huge driver of evolutionary variation.
An insertion is “often costly, but every once in a while you hit the jackpot, and a beneficial change arises that evolution preserves.
TBXT codes for a protein called "brachyury": Greek for “short tail” because mutations in it can lead to mice with shorter tails. At first glance, the ape-specific Alu element did not seem to cause any significant disruption in the gene, but on closer
inspection, Xia noticed a 2nd Alu-element lurking nearby. That element is present in monkeys & apes, but Xia realized that in apes the 2 Alus could stick together, forming a loop that would alter TBXT expression, so the resulting protein would be a bit
shorter than the original.
Hoekstra:
That insight “was very clever, it wouldn’t have jumped out at me as an obvious mutation to test.”
Indeed, Xia cs found that human embryonic stem-cells make 2 versions of the TBXT mRNA, one longer, one shorter.
Mouse cells OTOH only produce the longer transcript.
The researchers then used the genome editor CRISPR to remove one or the other Alu-element in human embryonic stem cells.
Losing either Alu-element made the shorter version of the mRNA disappear.
In other experiments to assess how the abbreviated ape-specific protein might influence tail development, Xia cs used CRISPR to make mice with a shortened version of TBXT.
The mice carrying both copies of the shortened gene didn’t survive, but those with 1 long & 1 short version were born with a variety of tail lengths: from none at all, to nearly normal, the group reports in a preprint posted last week on bioRxiv.
https://www.biorxiv.org/content/10.1101/2021.09.14.460388v1
That suggests to Xia cs that the shorter version of TBXT interferes with tail development.
Because the genetically altered mice had a mix of tail lengths, other genes must be working together to eliminate all tail development in apes & humans, but the ape-specific Alu insertion Xia noticed “was likely a critical event” c 25 Ma as great
apes diverged from other simians, says Itai Yanai (developme.geneticist NYU Langone Health, who helped coordinate the project).
The genetically modified mice also had unusu.high levels of neural tube problems, defects in the developing spinal cord.
Such birth defects (which produce spina bifida where the spinal cord doesn’t close, and anencephaly where parts of the brain & skull are missing) are fairly common in humans, affecting c 1 in 1000 newborns.
Yanai:
“We apparently paid a cost for the loss of the tail, and we still feel the echoes. We must have had a clear benefit for losing the tail, whether it was improved locomotion, or something else.”
Hoekstra:
That’s possible, but the defects seen in the mice could well have a different source than the human disorders.
Gagneux:
Overall, the Alu find is “a super interesting story”:
it leads to a wealth of questions, incl. how the shortened protein might help cause neural tube defects.
Some people are born with rudimentary tails, and sequencing their genomes might provide additional clues.
10.1126/science.acx9153

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)

On Wednesday, September 22, 2021 at 2:13:58 PM UTC-4, littor...@gmail.com wrote:

This article beautifully explains "how" hominoids c 25 Ma lost the tail.
The "why" is easier: they became bipedal in flooded/mangrove forests: wading upright + climbing arms overhead, google our TREE paper "Aquarboreal Ancestors".

The genetic basis of tail-loss evolution in humans and apes
Bo Xia cs 20121
https://doi.org/10.1101/2021.09.14.460388
The loss of the tail is one of the main anatomical evolutionary changes to have occurred along the lineage leading to humans & the “anthropomorphous apes”.
This morphological re-programming in the ancestral hominoids has been long considered to have accommodated a characteristic style of locomotion, and contributed to the evolution of bipedalism in humans.
Yet, the precise genetic mechanism that facilitated tail-loss evolution in hominoids remains unknown.
Primate genome sequencing projects have made possible the identification of causal links between genotypic & phenotypic changes, and enable the search for hominoid-specific genetic elements controlling tail development.
Here we present evidence that tail-loss evolution was mediated by the insertion of an individual Alu-element into the genome of the hominoid ancestor.
We demonstrate:
this Alu-element (inserted into an intron of the TBXT gene, also called T or Brachyury) pairs with a neighboring ancestral Alu-element encoded in the reverse genomic orientation, and leads to a hominoid-specific alternative splicing event.
To study the effect of this splicing event, we generated a mouse model that mimics the expression of human TBXT products by expressing both full-length & exon-skipped iso-forms of the mouse TBXT ortholog.
We found:
mice with this genotype exhibit the complete absence of a tail or a shortened tail, supporting the notion that the exon-skipped transcript is sufficient to induce a tail-loss phenotype, albeit with incomplete penetrance.
We further noted:
mice homozygous for the exon-skipped isoforms exhibited embryonic spinal cord malformations, resembling a neural tube defect, which affects ∼1/1000 human neonates.
We propose:
- selection for the loss of the tail along the hominoid lineage was ass.x an adaptive cost of potential neural tube defects,
- this ancient evolutionary trade-off may thus continue to affect human health today.

_______

‘Jumping gene’ may have erased tails in humans and other apes
— and boosted our risk of birth defects 21.9.21

Adding mobile DNA sequence to developmental gene short-circuits tail development in mice

Mammals from mice to monkeys have tails, but humans & great apes lack them. Now, researchers may have unearthed a simple genetic change that led to our abbreviated back end: an itinerant piece of DNA that leapt into a new chromosomal home, and changed

how great apes make a key developmental protein.

The finding also suggests the genetic shift came with a less visible & more dangerous effect: a higher risk of birth defects, involving the developing spinal cord.
Hopi Hoekstra (evol.biol.Harvard Univ.):
The work not only addresses an “inherently interesting question about what makes us human, but also provides new insights into how such evolutionary changes can occur. It’s beautiful work.”
Bo Xia (grad.student genome evolution NYU Grossman Sch.Medicine) wondered as a child why people didn’t have tails,
a tail-bone injury a few years ago renewed his curiosity.
A wealth of primate genomes has been sequenced in recent years, so he started to search for any ape-specific changes in genes known to play a role in tail development.
In a gene called TBXT, he found a strong suspect, a short DNA-insertion called an Alu element, present in all great apes, but missing in other primates.
Alu-sequences can move around the genome, and are sometimes called jumping genes or transposable elements.
Possibly remnants of ancient viruses, they’re common in the human genome, making up c 10 % of our DNA.
Sometimes an Alu-insertion interrupts a gene, and prevents its protein production,
in other cases, the elements have more complex effects, changing where or how a protein is expressed.
Pascal Gagneux (evol.biol.Univ.Calif. San Diego):
This makes them a huge driver of evolutionary variation.
An insertion is “often costly, but every once in a while you hit the jackpot, and a beneficial change arises that evolution preserves.
TBXT codes for a protein called "brachyury": Greek for “short tail” because mutations in it can lead to mice with shorter tails. At first glance, the ape-specific Alu element did not seem to cause any significant disruption in the gene, but on

closer inspection, Xia noticed a 2nd Alu-element lurking nearby. That element is present in monkeys & apes, but Xia realized that in apes the 2 Alus could stick together, forming a loop that would alter TBXT expression, so the resulting protein would be
a bit shorter than the original.

Hoekstra:
That insight “was very clever, it wouldn’t have jumped out at me as an obvious mutation to test.”
Indeed, Xia cs found that human embryonic stem-cells make 2 versions of the TBXT mRNA, one longer, one shorter.
Mouse cells OTOH only produce the longer transcript.
The researchers then used the genome editor CRISPR to remove one or the other Alu-element in human embryonic stem cells.
Losing either Alu-element made the shorter version of the mRNA disappear.
In other experiments to assess how the abbreviated ape-specific protein might influence tail development, Xia cs used CRISPR to make mice with a shortened version of TBXT.
The mice carrying both copies of the shortened gene didn’t survive, but those with 1 long & 1 short version were born with a variety of tail lengths: from none at all, to nearly normal, the group reports in a preprint posted last week on bioRxiv.
https://www.biorxiv.org/content/10.1101/2021.09.14.460388v1
That suggests to Xia cs that the shorter version of TBXT interferes with tail development.
Because the genetically altered mice had a mix of tail lengths, other genes must be working together to eliminate all tail development in apes & humans, but the ape-specific Alu insertion Xia noticed “was likely a critical event” c 25 Ma as great

apes diverged from other simians, says Itai Yanai (developme.geneticist NYU Langone Health, who helped coordinate the project).

The genetically modified mice also had unusu.high levels of neural tube problems, defects in the developing spinal cord.
Such birth defects (which produce spina bifida where the spinal cord doesn’t close, and anencephaly where parts of the brain & skull are missing) are fairly common in humans, affecting c 1 in 1000 newborns.
Yanai:
“We apparently paid a cost for the loss of the tail, and we still feel the echoes. We must have had a clear benefit for losing the tail, whether it was improved locomotion, or something else.”
Hoekstra:
That’s possible, but the defects seen in the mice could well have a different source than the human disorders.
Gagneux:
Overall, the Alu find is “a super interesting story”:
it leads to a wealth of questions, incl. how the shortened protein might help cause neural tube defects.
Some people are born with rudimentary tails, and sequencing their genomes might provide additional clues.
10.1126/science.acx9153

-
https://www.biorxiv.org/content/10.1101/2021.09.14.460388v1

25ma a jumping gene inserted into to tailmaking region, natural selection for shortened tail must have been strong since it carried risks of neural tube defects. Slow brachiation x slow bipedalism arboreal habit already incipiently in place, must have
occurred before hylobatids and great apes split and before morotopithecus. Great apes later readapted part-time quadrupedalism without tail, their forelimbs acting gyroscopically to maintain balance.

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)

DD'eDeN aka note/nickname/alas_my_loves wrote:

On Wednesday, September 22, 2021 at 2:13:58 PM UTC-4, littor...@gmail.com wrote:

This article beautifully explains "how" hominoids c 25 Ma lost the tail.
The "why" is easier: they became bipedal in flooded/mangrove forests: wading upright + climbing arms overhead, google our TREE paper "Aquarboreal Ancestors".

No evidence. Why would that explain

"We have presented evidence that tail-loss evolution in hominoids 2 was
driven
by the intronic insertion of an AluY element."

-
https://www.biorxiv.org/content/10.1101/2021.09.14.460388v1

25ma a jumping gene inserted into to tailmaking region, natural selection for shortened tail must have been strong since it carried risks of neural tube defects. Slow brachiation x slow bipedalism arboreal habit already incipiently in place, must have

occurred before hylobatids and great apes split and before morotopithecus. Great apes later readapted part-time quadrupedalism without tail, their forelimbs acting gyroscopically to maintain balance.


"Heterozygous mutations in the coding regions of the TBXT orthologs in tailed animals, such as mouse, Manx cat, dog and zebrafish, lead to the absence or reduced form of the tail, and homozygous mutants are typically not viable. Moreover, this particular Alu insertion is from the AluY subfamily, a relatively
‘young’ but not human-specific subfamily shared between the genomes of hominoids and Old World monkeys, the activity of which coincides with the evolutionary time when early hominoids lost their tails."

"We have presented evidence that tail-loss evolution in hominoids 2 was
driven
by the intronic insertion of an AluY element."

"Thus, while tail-loss evolution in hominoids may have been initiated by
the AluY
insertion, additional genetic changes may have then acted to stabilize the no-tail
phenotype in early hominoids (Fig. S8). Such a set of genetic events would explain
how a change to the AluY in modern hominoids would not result in the re-appearance of the tail."

"The specific evolutionary advantage for the loss of the tail is not
clear, though it
likely involved enhanced locomotion in a non-arboreal lifestyle. We can
assume
however that the selective advantage must have been very strong since the
loss
of the tail may have included an evolutionary trade-off of neural tube
defects, as demonstrated by the presence of spinal cord 6 malformations in
the Tbxt mutant
at E11.5 (Fig. S7)."

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)

On Friday, September 24, 2021 at 12:17:29 AM UTC-4, Primum Sapienti wrote:

DD'eDeN aka note/nickname/alas_my_loves wrote:

On Wednesday, September 22, 2021 at 2:13:58 PM UTC-4, littor...@gmail.com wrote:

This article beautifully explains "how" hominoids c 25 Ma lost the tail. >> The "why" is easier: they became bipedal in flooded/mangrove forests: wading upright + climbing arms overhead, google our TREE paper "Aquarboreal Ancestors".

No evidence. Why would that explain

"We have presented evidence that tail-loss evolution in hominoids 2 was driven
by the intronic insertion of an AluY element."

-
https://www.biorxiv.org/content/10.1101/2021.09.14.460388v1

25ma a jumping gene inserted into to tailmaking region, natural selection for shortened tail must have been strong since it carried risks of neural tube defects. Slow brachiation x slow bipedalism arboreal habit already incipiently in place, must

have occurred before hylobatids and great apes split and before morotopithecus. Great apes later readapted part-time quadrupedalism without tail, their forelimbs acting gyroscopically to maintain balance.

"Heterozygous mutations in the coding regions of the TBXT orthologs in tailed
animals, such as mouse, Manx cat, dog and zebrafish, lead to the absence or reduced form of the tail, and homozygous mutants are typically not viable. Moreover, this particular Alu insertion is from the AluY subfamily, a relatively
‘young’ but not human-specific subfamily shared between the genomes of hominoids and Old World monkeys, the activity of which coincides with the evolutionary time when early hominoids lost their tails."

"We have presented evidence that tail-loss evolution in hominoids 2 was driven
by the intronic insertion of an AluY element."

"Thus, while tail-loss evolution in hominoids may have been initiated by
the AluY
insertion, additional genetic changes may have then acted to stabilize the no-tail
phenotype in early hominoids (Fig. S8). Such a set of genetic events would explain
how a change to the AluY in modern hominoids would not result in the re-appearance of the tail."

"The specific evolutionary advantage for the loss of the tail is not
clear, though it
likely involved enhanced locomotion in a non-arboreal lifestyle. We can assume
however that the selective advantage must have been very strong since the loss
of the tail may have included an evolutionary trade-off of neural tube defects, as demonstrated by the presence of spinal cord 6 malformations in the Tbxt mutant
at E11.5 (Fig. S7)."

-
Thanks, I missed the manx cat ref. But I question their "non-arboreal" claim. Arboreal slow-brachiation and arboreal slow-bipedalism preceded tail loss, see many tailed monkeys that have some swinging and reaching above branches with a few bipedal steps.
Whereas terrestrials always retain at least short tails, birds too, they always have dense body coverings because they have no bug swatting tails. 25ma hominoids spent very little time on the ground, maybe like today's sloths which have short stubby
tails.

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)

Op vrijdag 24 september 2021 om 09:06:41 UTC+2 schreef DD'eDeN aka note/nickname/alas_my_loves:

This article beautifully explains "how" hominoids c 25 Ma lost the tail.
The "why" is easier:
they became bipedal in flooded/mangrove forests: wading upright + climbing arms overhead,
google our TREE paper "Aquarboreal Ancestors".

...

... arboreal slow-bipedalism ...

:-DDD

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)

On Saturday, September 25, 2021 at 3:16:16 AM UTC-4, littor...@gmail.com wrote:

Op vrijdag 24 september 2021 om 09:06:41 UTC+2 schreef DD'eDeN aka note/nickname/alas_my_loves:
This article beautifully explains "how" hominoids c 25 Ma lost the tail.
The "why" is easier:
they became bipedal in flooded/mangrove forests: wading upright + climbing arms overhead,
google our TREE paper "Aquarboreal Ancestors".
...

... arboreal slow-bipedalism ...

:-DDD

flooded forest = swamp forest = great apes
shallow crystalline streams in uplands = rainforest continuous canopy = hylobatids (aerial), Homo (terrestrial)
Tail loss 25ma = arboreal slow orthograde bimanual/bipedal locomotion
Mermaids aren't bipedal, meine kleine tochter.
Sifakas and siamangs avoid open water and are obligate bipeds.

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)

On Saturday, September 25, 2021 at 2:26:55 PM UTC-4, DD'eDeN aka note/nickname/alas_my_loves wrote:

On Saturday, September 25, 2021 at 3:16:16 AM UTC-4, littor...@gmail.com wrote:

Op vrijdag 24 september 2021 om 09:06:41 UTC+2 schreef DD'eDeN aka note/nickname/alas_my_loves:
This article beautifully explains "how" hominoids c 25 Ma lost the tail. The "why" is easier:
they became bipedal in flooded/mangrove forests: wading upright + climbing arms overhead,
google our TREE paper "Aquarboreal Ancestors".
...

... arboreal slow-bipedalism ...

:-DDD

flooded forest = swamp forest = great apes
shallow crystalline streams in uplands = rainforest continuous canopy = hylobatids (aerial), Homo (terrestrial)
Tail loss 25ma = arboreal slow orthograde bimanual/bipedal locomotion Mermaids aren't bipedal, meine kleine tochter.
Sifakas and siamangs avoid open water and are obligate bipeds.

-
Dino ran while swinging tail as humans run by swinging arms.

https://phys.org/news/2021-09-simulations-bipedal-dinosaurs-swung-tails.html

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)

On Saturday, September 25, 2021 at 8:15:57 PM UTC-4, DD'eDeN aka note/nickname/alas_my_loves wrote:

On Saturday, September 25, 2021 at 2:26:55 PM UTC-4, DD'eDeN aka note/nickname/alas_my_loves wrote:

On Saturday, September 25, 2021 at 3:16:16 AM UTC-4, littor...@gmail.com wrote:

Op vrijdag 24 september 2021 om 09:06:41 UTC+2 schreef DD'eDeN aka note/nickname/alas_my_loves:
This article beautifully explains "how" hominoids c 25 Ma lost the tail. The "why" is easier:
they became bipedal in flooded/mangrove forests: wading upright + climbing arms overhead,
google our TREE paper "Aquarboreal Ancestors".
...

... arboreal slow-bipedalism ...

:-DDD

flooded forest = swamp forest = great apes
shallow crystalline streams in uplands = rainforest continuous canopy = hylobatids (aerial), Homo (terrestrial)
Tail loss 25ma = arboreal slow orthograde bimanual/bipedal locomotion Mermaids aren't bipedal, meine kleine tochter.
Sifakas and siamangs avoid open water and are obligate bipeds.

-
Dino ran while swinging tail as humans run by swinging arms.

https://phys.org/news/2021-09-simulations-bipedal-dinosaurs-swung-tails.html

-

https://youtu.be/cEItmb_a20M

Bimanual palmigrade orthograde runner with caudal regression syndrome

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)