Such is the case with almost all mammals, from mice to elephants, but humans and other great apes lack it — namely, him.
New genetic research has brought enlightenment into the mystery of why man does not have this limb suitable for balancing. All we were left with was a tail bone as a hint that our distant ancestors still had some kind of tail.
An as yet peer-reviewed study has been published on Arxiv.
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A graduate student at New York University Bo Xia setvi monkey genes that have previously been known to play a role in tail formation.
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Xia found a short DNA fragment in the tbxt gene that is present in all great apes, but not in other primates. This fragment is a jumping gene, also known as a so-called alu element.
Alu is the most common part of the human genome and makes up about ten percent of it. They are sometimes called jumping genes because they have the rare ability to “jump” to new places inherit.
Hopping a large gene fragment means that each variant is very likely to be unique. Therefore, similar alu-elements in organisms are an almost certain sign of a common ancestor.
It is known in the past that the tbxt gene has a code for a particular protein, the altered production of which often causes short-tailed tails, for example in mice. However, the alu element found by Xia did not appear to affect the production of that protein.
However, Xia soon found another alongside the original alu element, and together these two jumping gene fragments appear to be at least partly to blame for our tail’s absence.
The researchers continued the experiments by modifying both human stem cells and the genome of experimental mice with crispr modification, which can be used to quickly remove or add gene fragments.
It was found that the tbxt genes affecting the tail in human stem cells have two different messengers, long and short. Mice naturally have only a long variant.
The messenger is a kind of cell-produced set of instructions that tells the body what kind of proteins the body needs to produce.
When the researchers tested a shorter rna version of humans in mice, the result varied.
If the mice had two pairs of short versions borrowed from humans, they were not viable. If, on the other hand, the mice had both a long and a short version, it only had a variable effect on tail length. Some test mice had an almost normal tail and others a very short one.
The result led the researchers to conclude that a shorter snippet does indeed affect tail formation.
However, some of the mice still had an almost normal tail. Therefore, scientists speculate that other genes must also play a part in the fact that we have lost our tail.
The jumping gene fragment was still probably an important factor in tail loss, according to Xia. It happened at about the same time as great apes differed from other primates more than 25 million years ago, says the geneticist Itai Yanai Sciencejournal.
Source: Tiede by www.tiede.fi.
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