Humans, unlike most other mammals, lack tails. This seemingly small difference has significant implications for our evolution and development. The loss of our tails happened millions of years ago, a consequence of a specific genetic mutation that impacted our ancestors.
You might think that our transition to bipedalism, walking upright on two legs, is the main reason we lost our tails. After all, tails are helpful for balance in four-legged animals. While bipedalism certainly played a role, scientists have discovered a more precise genetic mechanism behind this evolutionary change.
In 2023, researchers found that a specific type of “jumping gene,” called an Alu element, inserted itself into the TBXT gene, which is responsible for tail length in other animals. This Alu element is present in hominoids, which include humans and great apes, but not in monkeys.
The Alu element disrupted the TBXT gene, preventing it from producing the proteins necessary for tail development. Experiments with genetically modified mice confirmed this theory. Mice with the Alu insertion in their TBXT genes had shorter tails or no tails at all.
So, while bipedalism likely contributed to the evolutionary advantage of a tailless body, the loss of tails was primarily driven by a specific genetic mutation that disrupted the TBXT gene. This mutation was a significant change in our evolutionary history, with implications for both our skeletal structure and the development of the neural tube, which forms the brain and spinal cord.
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- How does the Alu element affect other genes in the human genome?
- What are the other potential consequences of this genetic mutation, beyond the loss of tails?
- What are the implications of this discovery for our understanding of evolution?
- How does this discovery change our understanding of the role of “junk DNA” in our genome?
- Are there any other examples of “jumping genes” influencing human evolution?