A new study explores the function of one part of “junk” DNA and shows that at least one family of transposons — ancient viruses that have invaded our genome by the millions — plays a href=”https://www.eurekalert.org/news-releases/931923″>a critical role in viability in the mouse, and perhaps in all mammals:
When the researchers knocked out a specific transposon in mice, half their mouse pups died before birth.
This is the first example of a piece of “junk DNA” being critical to survival in mammals.
In mice, this transposon regulates the proliferation of cells in the early fertilized embryo and the timing of implantation in the mother’s uterus. The researchers looked in seven other mammalian species, including humans, and also found virus-derived regulatory elements linked to cell proliferation and timing of embryo implantation, suggesting that ancient viral DNA has been domesticated independently to play a crucial role in early embryonic development in all mammals.
According to senior author Lin He, UC Berkeley professor of molecular and cell biology, the findings highlight an oft-ignored driver of evolution: viruses that integrate into our genome and get repurposed as regulators of host genes, opening up evolutionary options not available before.
There is no “junk” DNA.