Reactive oxygen species (ROS), or oxygen radicals, have been identified as major contributors to signs of premature aging, increased cancer prevalence linked to inflammation-associated syndromes and a variety of human diseases. Now scientists at the University of California, San Diego Branch of the Ludwig Institute for Cancer Research (LICR) have identified a key network of DNA repair and cell cycle control genes in yeast that prevents the deleterious effects of ROS.
"DNA repair and cell cycle control mechanisms are important guardians against cancerous changes in human cells," says Dr. Richard Kolodner, LICR Member and senior author of the study. "However, the effects of ROS on these cellular responses have not been well characterized. Weve now identified a group of genes that cooperate to suppress DNA mutations and the genome rearrangements that are the hallmarks of cancer cells that occur in response to ROS."
Dr. Kolodner and lead author, Meng-Er Huang, generated various yeast strains each with a mutation in the TSA1 gene, which results in increased production of ROS, plus a mutation in one or more genes involved in DNA repair or cell cycle control. Cell survival and accumulation of DNA mutations and gross chromosomal rearrangements in each strain were then analysed to identify genes that cooperate to prevent the deleterious effects of ROS and promote normal cell survival.
Sarah L. White | EurekAlert!
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