Department of Biology

Drosophila melanogaster—the common fruit fly—is widely used in laboratory experiments. But what Rochester researchers found when examining the guts of fruit flies in the wild bears little resemblance to what is seen in the lab.

There are many examples of DNA damage being associated with aging, but never has a reduction in DNA damage been shown to extend lifespan. Rochester research has made this connection, and identified an enzyme that can be targeted to reduce that damage.

Researchers who specialize in the study of aging have identified a protein that may serve as a first responder, activating a “longevity gene” known as sirtuin 6 and setting in motion a cascade of molecular first responders to repair damaged DNA.

Four Rochester researchers are among the latest recipients of the National Science Foundation’s most prestigious award for junior faculty members.

Students submitted 63 nominations, and a Student Association Government academic affairs legislature committee deliberated and selected the winners.

Nate Powers '16, Ka’dya Donadelle, and Seth Mason ’16 and were among the 35 students honored on Wednesday, April 20, by the Rochester Area Colleges Continuing Education.

LISTEN: David Goldfarb, professor of biology, researches yeast as a model organism for understanding the aging process in humans. Why does this essential ingredient in bread and beer make a good research specimen?

“There’s an explosion of insect genome sequencing right now,” said Jack Werren, a professor of biology and a member of the research team. “But the bed bug is particularly interesting because it’s a human parasite, a major pest, and has a unique biology.”

Naked mole rats are small, hairless, subterranean rodents that have never been known to get cancer despite having a 30-year lifespan. A new protein discovered by biologist Vera Gorbunova may help explain why.

Biology researchers Vera Gorbunova and Andrei Seluanov report that the “jumping genes” in mice become active as the mice age when a multi-function protein stops keeping them in check in order to take on another role. A protein called Sirt6 is needed to keep the jumping genes—technically known as retrotransposons—inactive.