The researchers discovered that even after the stress associated with DNA replication, surviving, non-dividing, resting, old stem cells retained molecular tags on DNA-wrapping histone proteins, a feature often associated with DNA damage. However, the researchers determined that these old survivors could repair induced DNA damage as efficiently as young stem cells.
"Old stem cells are not just sitting there with damaged DNA ready to develop cancer, as it has long been postulated" Passegu said.
But not all was well in the old, surviving stem cells. The molecular tags accumulated on genes needed to make the cellular factories known as ribosomes. The ribosomes make all the cell's proteins. Passegu will further explore the consequences of reduced protein production as part of her ongoing research.
"Everybody talks about healthier aging," Passegu added. "The decline of stem-cell function is a big part of age-related problems. Achieving longer lives relies in part on achieving a better understanding of why stem cells are not able to maintain optimal functioning."
Passegu hopes that it might be possible to prevent declining stem-cell populations by developing a drug to prevent the loss of the helicase components needed to faithfully unwind and replicate DNA, thereby avoiding immune-system failure.
|Contact: Jeffrey Norris|
University of California - San Francisco