Transposons play a significant role in aging and disease, researcher says.
If you’ve ever seen a petunia with artfully variegated petals, then you’ve seen transposons at work. The flower’s showy color patterns are due to transposable elements, or DNA sequences that can move locations within a genome. Yet when it comes to transposons’ effects on humans, the results might not be as lovely or desirable.
As researchers learn more about these so-called mobile genetic elements, they’ve found increasing evidence that transposons influence and even promote aging and age-related diseases like cancer as well as neurogenerative and autoimmune disorders, says John Sedivy, PhD, a professor of biology and director of the Center on the Biology of Aging at Brown. Sedivy is the corresponding author of a new review article in Nature that discusses the latest thinking and research around transposons.
“Let’s put it this way: These things can be pretty dangerous,” Sedivy says. “If they are uncontrolled, and there are many examples of that, transposons can have profound consequences on most forms of life that we know of.”
Since the dawn of life, the researchers noted, transposons have coevolved with their host genomes, but it’s been more of a competitive existence than a peaceful one, earning them the nicknames of “junk DNA” and “molecular parasites.” Transposons were first discovered in corn by the Nobel prize-winning geneticist Barbara McClintock, PhD, in the 1940s, who also found that depending on where they inserted into a chromosome, they could reversibly alter the expression of other genes.
It is now quite apparent that the genomes of virtually all organisms, including humans, contain repetitive sequences generated by the activity of transposons. When these elements move from one chromosome or part of a chromosome to another, they amplify and increase their presence in genomes, sometimes to dramatic levels. According to Sedivy, “about half of the human genome is due to the activity of these molecular parasites.” Their unregulated activity can have long-term benefits by increasing genetic diversity in organisms, but in most cases the chaos degrades cell function, such as by disrupting useful genes.
Most of what is known about transposons, Sedivy says, comes from genome sequence data that shows their activity in the germline, or throughout successive generations of an organism. However, recent research, including from Sedivy and other scientists at Brown, has revealed a wealth of information on transposon activity during the lifetime of a single individual, as well.
In an interview, Sedivy discussed the mechanisms driving transposons, how their activity influences and promotes age-related tissue degeneration and disease—and what can be done to fight back.
