Telomere dysfunction drives increased mutation by error-prone polymerases Rev1 and zeta in Saccharomyces cerevisiae.
Using a model system, we have shown that replicative senescence is accompanied by a 16-fold increase in base substitution and frameshift mutations near a chromosome end. The increase was dependent on error-prone polymerases required for the mutagenic response to DNA lesions that block the replication fork.
Meyer
Damon H
DH
Division of Molecular Biology, Beckman Research Institute of the City of Hope, Duarte, California 91010-0269, USA.
Bailis
Adam M
AM
D026923:Amino Acid Transport Systems, Basic / Q000235:genetics*; D002455:Cell Division / Q000235:genetics*; D015321:Gene Rearrangement / Q000235:genetics; D016296:Mutagenesis; D009713:Nucleotidyltransferases / Q000235:genetics*; D017354:Point Mutation / Q000235:genetics*; D012441:Saccharomyces cerevisiae / Q000166:cytology / Q000235:genetics*; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics*; D019098:Telomerase / Q000235:genetics; D016615:Telomere / Q000235:genetics*; D000099270:Y-Family DNA Polymerases
D026923:Amino Acid Transport Systems, Basic; D009713:Nucleotidyltransferases; D029701:Saccharomyces cerevisiae Proteins; D019098:Telomerase; C502212:CAN1 protein, S cerevisiae; C100951:REV1 protein, S cerevisiae; D000099270:Y-Family DNA Polymerases; C509185:EST2 protein, S cerevisiae