Collaborations between Johns Hopkins and National Taiwan University researchers have successfully manipulated the life span of common, single-celled yeast organisms by figuring out how to remove and restore protein functions related to yeast aging.
A chemical variation of a "fuel-gauge" enzyme that senses energy in yeast acts like a life span clock: It is present in young organisms and progressively diminished as yeast cells age.
In a report in the September 16 edition of Cell, the scientists describe their identification of a new level of regulation of this age-related protein variant, showing that when they remove it, the organism's life span is cut short and when they restore it, life span is dramatically extended.
In the case of yeast, the discovery reveals molecular components of an aging pathway that appears related to one that regulates longevity and lifespan in humans, according to Jef Boeke, Ph.D., professor of molecular biology, genetics and oncology, and director of the HiT Center and Technology Center for Networks and Pathways, Johns Hopkins University School of Medicine.
"This control of longevity is independent of the type described previously in yeast which had to do with calorie restriction," Boeke says. "We believe that for the first time, we have a biochemical route to youth and aging that has nothing to do with diet." The chemical variation, known as acetylation because it adds an acetyl group to an existing molecule, is a kind of "decoration" that goes on and off a protein in this case, the protein Sip2 much like an ornament can be put on and taken off a Christmas tree, Boeke says. Acetylation can profoundly change protein function in order to help an organism or system adapt quickly to its environment. Until now, acetylation had not been directly implicated in the aging pathway, so this is an all-new role and potential target for prevention or treatment strategies, the researchers say.
|Contact: Audrey Huang|
Johns Hopkins Medical Institutions