A combined team of researchers from the Buck Institute of Research on Aging and the University of Washington have isolated 238 genes which when removed, increase the replicative lifespan (RLS) of Saccharomyces cerevisiae yeast cells. The study took ten years of effort and the researchers called it “exhaustive.”
You may have probably read reverse aging in human cell lines in which genes’ – CGAT and SHMT2 – glycine production in mitochondria, when altered, induced defects or restore mitochondrial function in the fibroblast cell lines. However, this new research involves deleting certain genes from yeast strains and shows how this action influences the aging process.
For the study, the researchers performed a systematic analysis of 4,698 yeast strains from which they painstakingly delete single cell from each. They found that when any of these 238 genes are not present, the yeast’s lifespan goes up and 189 of these genes have been linked to aging.
“This study looks at aging in the context of the whole genome and gives us a more complete picture of what aging is,” said Brian Kennedy, PhD, lead author and the Buck Institute’s president and CEO. “It also sets up a framework to define the entire network that influences aging in this organism.”
According to the study, among the mechanisms of aging identified, deleting a gene called LOS1 produced particularly stunning results. Researchers say deleting this gene alone robustly extends lifespan of the yeast by 60 percent, reports the Telegraph. LOS1 is a nuclear pore protein which helps bring amino acids to ribosome to build proteins. LOS 1 is influenced by mTOR, genetic master switch that is already associated with caloric restriction and increased lifespan.
“Calorie restriction has been known to extend lifespan for a long time.” said Dr. Kennedy. “The DNA damage response is linked to aging as well. LOS1 may be connecting these different processes.”
You may question what has this yeast study got to so with humans. Well, researchers have an answer for that. According to them, many of the anti-aging pathways associated with yeast genes are maintained all the way to humans. A number of the age-extending genes they identified are also found in C. elegans roundworms, this indicates that these mechanisms can be maintained in higher organisms as well.
“Almost half of the genes we found that affect aging are conserved in mammals,” said Dr. Kennedy. “In theory, any of these factors could be therapeutic targets to extend healthspan. What we have to do now is figure out which ones are amenable to targeting.”
Researchers hope this research would open roads to new therapies and would eventually provide new genomic targets that could improve human health. The results of the study was published in the journal Cell Metabolism – A Comprehensive Analysis of Replicative Lifespan in 4,698 Single-Gene Deletion Strains Uncovers Conserved Mechanisms of Aging.