Millions of years ago humans had an external tail. Why did we lose it?

In the animal world, the tail is an essential part of the body. howler monkeys (Sunni Watta), for example, they use them to grasp or grasp objects while in trees. Some other animals use it to regulate temperature, and (in the case of lizards) it even serves as a distraction to escape predators. Long ago, humans had an external tail. It is thought that we lost it during evolution, about 25 million years ago, when the human lineage separated from the ancient Old World monkeys. For years, there has been speculation that the loss of the tail was key to the emergence of orthopedic locomotion and bipedal locomotion (with the torso upright and on two limbs, in this case, legs), which is fundamental to life as humans know it today. . However, the genetic mechanism that facilitated the development of tail loss remains unknown. So far.

New research published in nature (which took more than two years to accept) threw some interesting light on the subject, through a series of experiments on mice. The researchers initially analyzed 31 human genes and their primate equivalents whose mutations are associated with the absence of an external tail. Finding no mutations there, they added genes from mice with mutations that cause tail reduction to their analysis, and systematically looked for genetic differences in regions near the genes. However, they discovered thousands of variants, and none of them had strong evidence that they contributed to the development of tail loss, so they tried other things.

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By examining several specific variables, scientists found an element called… Aluminium In a gene called TBXT Which is related to the development of the tail. This element appears to have very interesting properties, such as its presence specifically in hominins (a group that includes humans and close relatives), its presence in a gene known for its role in tail formation, and its close relationship with another element, Alu (which we will return to later). Moreover, their introduction in time coincides with the period in which early hominins lost their tails. What has most interested scientists is that the TBXT gene is essential for embryonic development, and mutations in this gene in animals with tails, such as mice and cats, lead to the absence or reduction of the tail, which suggests that the Alu element found in the TBXT gene could be related to the loss of the tail. In hominins.

Now, scientists have discovered that this Alu element forms a structure with another element they found in the opposite direction in the same TBXT gene. The two Alu elements (called AluY and AluSx1 to differentiate them) form a special structure that affects how the TBXT gene is transcribed over time. This results in a different version of the gene, called TBXT Δexon6, which appears to be associated with tail reduction or loss during embryonic development in hominins, including humans. The researchers confirmed the presence of this version in humans and its absence in mice (which have tails), which indicates a link between this genetic process and the development of tail loss.

But how is this theory proven? Scientists have created a special mouse using a technology called CRISPR. This mouse had one copy of the TBXT gene, which expresses the full version of the gene, and an alternative copy called TBXT Δexon6 (which would be responsible for the loss of the tail). Mice with this newer version of the gene showed different tail shapes, including some without tails and others with shorter tails. Specifically, 21 out of 63 showed different types of tails, while none of their colleagues with the normal gene had these tail changes. What's interesting, the scientists say in their study, is that this difference in the tail was inconsistent between mice with the particular version of the gene. Parents with short tails or no tails produced mice with normal tails, and those with normal tails produced mice with different types of tails.

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These results indicate that the presence of the alternative version of the gene, TBXT Δexon6, is sufficient to cause tail loss or alteration in mice. The researchers concluded that the introduction of the AluY element may have caused the reduction or partial loss of the tail in early human ancestors. However, other genetic changes may have stabilized tailless humans. This is important because it indicates that a future change in the AluY element in modern hominins would not lead to the tail appearing again.

The specific evolutionary pressures associated with tail loss in hominins are unclear, although they are likely involved in increased locomotion in the transition to a non-arboreal lifestyle. That is, in adapting to living less in trees and more on the ground. Reduction or loss of the tail could have provided advantages for bipedal locomotion and efficient locomotion in open environments. However, scientists suggest that the loss of the tail could have been accompanied by a compensation that represented an evolutionary advantage.

The key is in what is known as the neural tube. In simple terms, it is like a structure that helps form the brain and spinal cord, including humans. In the research, when mice were called a copy of the TBXT gene Δexon6 TPCST (associated with tail loss) had problems closing this neural tube. What's amazing is that when hominins lost their tails, those defects in neural tube design that the researchers saw in mice could have somehow been compensated for by evolution to ensure adaptability and evolutionary success. This is key because it suggests that evolutionary compensation associated with tail loss, which occurred about 25 million years ago, could have an impact on human health to this day.