The discovery, published in Nature, pinpoints a mobile genetic element—often called a jumping gene—that embedded itself into the genome of our ancestors. While most repetitive DNA sequences remain inert, this specific insertion interacted with the TBXT gene to produce two distinct forms of ribonucleic acid. This disruption proved sufficient to halt tail development, a feature that distinguishes humans and great apes from their monkey counterparts.
To confirm the hypothesis, the team introduced the AluY sequence into mice. The resulting offspring exhibited either significantly shortened tails or none at all. However, the study suggests this evolutionary milestone may have carried a biological cost. Researchers observed a correlation between the tail-loss mutation and an increased incidence of neural tube defects. Dr. Itai Yanai noted that this suggests a prehistoric trade-off, where the anatomical shift toward a tailless body plan potentially introduced the susceptibility to conditions like spina bifida.





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