Roundworms (C. elegans) born without the protien called arrestin lived a third longer than normal, while worms with triple the amount of the protein cut their lives short by one-third.
The findings could have implications for humans, because most proteins in worms have human counterparts, according to study researcher Jeffrey L. Benovic, professor and chair of the Department of Biochemistry and Molecular Biology at Thomas Jefferson University. For instance, the human version of one of these longevity proteins is PTEN, a well-known tumor suppressor.
“The links we have found in worms suggest the same kind of interactions occur in mammals although human biology is certainly more complicated,” Benovic said. “We have much work to do to sort out these pathways, but that is our goal.”
The roundworm is a useful model for studying human diseases and other aspects of human biology, because the worm is much simpler than humans but also has similarities to us. The worm, for example, has one arrestin gene, whereas humans have four. Worms only have 302 neurons compared with the 100 billion or so neurons in the human brain. In addition, their short lifespans of two to three weeks allows for timely observation of effects on longevity.
Taking advantage of this simplicity, Benovic and Aimee Palmitessa, a postdoctoral research fellow at the university, deleted the single arrestin gene in worms to see what would happen. To Palmitessa’s surprise, these worms lived significantly longer. She also found that over-expressing arrestin in worms shortened their lifespan.
“A little less arrestin is good – at least for worms,” Benovic said.