The lack of tails in humans, which are a characteristic peculiar to most vertebrate animals, has always been an enigma for scientists. 

According to CNN, although tails provide a wide range of functions including balance and communication, humans and their closest relatives among the apes, the great apes, separated ways from the rest of the primates around 25 million years ago, forgoing the feature. 

Although formerly linked to the change to bipedalism, these genetic prompts in a primate taillessness had been obscure.

In contrast to their years of research showing that the sequence Alu element is non-functional or “junk DNA,” researchers identified it as critical to this phenomenon in a groundbreaking study. 

Through their study, they found that the Alu element’s insertion is only exclusive to hominoids (great apes and humans), which is responsible for tail length. Through gene editing in mice during a four-year time period, scientists have demonstrated that Alu insertions into TBXT alter protein production which results in individual variations in tail length.

Lead author of the study, Bo Xia, a fellow of the Broad Institute of MIT and Harvard University, emphasized the importance of this finding which is the first genetic explanation for human and great ape tail loss. This particular Alu element out of millions in the human DNA caught my attention for the possible effect it would have on the TBXT gene function.

However, beside making the genetic basis of tail loss visible, the experiment may have implications for human fetal development, especially for neural tube defects like spina bifida. 

The results upset notions of “junk DNA” and emphasize the dynamic interactions between genes, development, and evolutionary processes in shaping the human traits.