A new study increases and strengthens the links that have previously led scientists to propose the "transposon theory of aging." Transposons are rogue elements of DNA that break free in aging cells and rewrite themselves elsewhere in the genome, potentially creating lifespan-shortening chaos in the genetic makeups of tissues. As cells get older, prior studies have shown, tightly wound heterochromatin wrapping that typically imprisons transposons becomes looser, allowing the transposons to slip out of their positions in chromosomes and move to new ones, disrupting normal cell function. Meanwhile, scientists have shown that potentially related interventions, such as restricting calories or manipulating certain genes, can demonstrably lengthen lifespans in laboratory animals. "In this report the big step forward is towards the possibility of a true causal relationship," said Dr. Stephen Helfand, Brown University professor of biology and senior author of a new study published online on August 24, 2016 in PNAS. The open-access article is titled “An Accelerated Assay for the Identification of Lifespan-Extending Interventions in Drosophila melanogaster.” "So far there have been associations and suggestions that to all of us make sense, but the difference in science is that you need the data to back up your opinion." The new results, achieved under the leadership of faculty investigator Dr. Jason Wood, come from several experiments that are thorough and direct in connecting the dots among weakening heterochromatin, increased transposon expression, aging, and lifespan. In one set of experiments, the team visually caught transposable elements in the act of jumping around in fruit flies as they aged.
Login Or Register To Read Full Story