Home Science “Jumping genes” explain why humans don’t have tails

“Jumping genes” explain why humans don’t have tails

“Jumping genes” explain why humans don’t have tails

The Loss of tail It is a characteristic feature of monkeys and may have influenced the upright walking style. Most monkeys have it, in fact it is a way to distinguish them from monkeys. This trait or phenotype is common to all, suggesting that their loss coincided with later splitting from the last common ancestor.

Researchers at NYU Langone Health (USA) are leading a study in which they explain that the insertion of a type of mobile genetic sequence that moved through the genome during evolution, known as transposable element or “jumping genes” – DNA sequences with the ability to change position – could be linked to tail loss.

“We offer for the first time a plausible scenario for the genetic mechanism that led to tail loss in our ancestors.” “It is surprising that such a large anatomical change can be caused by such a small genetic change,” the scientist tells SINC . Itai Yanai, scientific director of NYU Applied Bioinformatics Laboratories. The article will be published in the magazine Nature.

It is surprising that such a large anatomical change can be caused by such a small genetic change.

Itai Yanai of NYU Langone Health

They analyzed 140 genes related to the evolution of the vertebrate tail, looking for changes that may have caused the loss of the tail in hominoids. To this end, the work began by comparing the key candidate genes in the genomes of several primate species, initially focusing on exons (regions of DNA that code for proteins).

However, since this approach was unsuccessful, they decided to extend the study to the non-protein coding regions located in the genes themselves, called introns. They discovered that a primate-specific type of transposable element, the so-called Alu5 element, is inserted into a Intron of the TBXT gene (associated with tail development in animals).

To test this theory, they generated Mouse models which expressed different forms of the TBXT gene, both the full and the new isoform with exon skipping (which is induced in hominoids by the insertion of the Alu element). The authors found that in both cases the mice had either no tail or a shorter tail.

We identify a change in the TBXT gene that plays a critical role during embryonic development and supports the development of a tail in nonhominoids

Itai Yanai

“We have identified a change in the TBXT gene, which plays a crucial role during embryonic development and supports the development of a tail in non-hominoids. The genetic change we observed consists of a short genetic jump (the Alu element) that lands on a non-coding part of a gene. We show that its proximity to another Alu element leads to the emergence of a different type of protein that normally plays a role in tail development. If we make a similar mutation in the mouse, it loses its mutation,” explains the scientist.

A loss due to illness

In addition, they discovered that mice expressing the exon-skipped Tbxt isoform can develop neural tube defects, a condition that affects one in 1,000 human newborns.

“A condition similar to human spina bifida (a type of neural tube defect) was also observed in some mice that had lost their tails. “This suggests that the evolutionary pressure to lose our tail was so great that even though we created the potential for this condition, we still lost it,” argues the expert.

A condition similar to human spina bifida was also observed in some mice that had lost their tails.

Itai Yanai

“We believe that since the tail is so fundamental to vertebrates, a simple mutation may have caused the observed defects,” he says. For the scientist, this connection with a greater probability of neural tube defects in humans and monkeys needs to be studied to collect more information and verify whether it is correct.

Reference:

Itai Yanai et al. “On the genetic basis of tail loss development in humans and monkeys.” Nature.

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