April 24, 2014
CHAPEL HILL, N.C. The evidence for what causes aging has typically been limited to the study of a single organism's lifespan; our cells divide many times throughout our lives and eventually cause organs and our bodies to age and break down. But new research from the UNC School of Medicine suggests that how we age might depend on cellular interactions that we inherit from ancestors throughout many generations.
By studying the reproductive cells of nematodes tiny worms found in soil and compost bins Shawn Ahmed, PhD, an associate professor of genetics, identified the Piwi/piRNA genome silencing pathway, the loss of which results in infertility after many generations. He also found a signaling pathway a series of molecular interactions inside cells that he could tweak to overcome infertility while also causing the worms to live longer adult lives.
The research, in collaboration with researchers at the University of Cambridge and described in a paper published in the journal Cell Reports, suggests that it's possible to manipulate the aging process of progeny before they're even born.
The finding gives scientists a deeper understanding of what may govern aging and age-related diseases, such as some cancers and neurodegenerative conditions.
Typically, nematodes produce about 30 generations in a matter of months and remain fertile indefinitely. Ahmed and colleagues found that a mutation in the Piwi/piRNA cellular pathway of germ cells gradually decreased the worms' ability to reproduce as the mutation was passed down through the generations and eventually caused complete sterility. But when Ahmed's team manipulated a different protein DAF-16/FOXO the nematodes overcame the loss of the Piwi pathway. The worms did not become sterile; generations of worms reproduced indefinitely, achieving a sort of generational immortality. Moreover, it has been well established that DAF-16/FOXO plays a role in ne
|Contact: Mark Derewicz|
University of North Carolina Health Care