title: The availableSRL3deletion strain ofSaccharomyces cerevisiaecontains a truncation of DNA damage tolerance protein Mms2: Implications for Srl3 and Mms2 functions.
abstract: A screen of the commercially available collection of haploid deletion mutants ofSaccharomyces cerevisiaefor spontaneous mutator mutants newly identified a deletion ofSRL3. This gene had been previously isolated as a suppressor of lethality of checkpoint kinase deletions if overexpressed. We found DNA damage sensitivity and extended checkpoint arrests to be associated with this strain. However, when crossed to wild-type, a mutant gene conferring these phenotypes was found to segregate from theSRL3deletion. The mutation was identified as a C-terminal truncation of Mms2, an E2 ubiquitin conjugating enzyme involved in error-free replicative bypass of lesions. This confirmed an earlier report that Mms2 may be required to restrain error-prone polymerase ζ activity and underscored that residues of the C-terminus are necessary for Mms2 function. Srl3, on the other hand, does not appear to influence DNA damage sensitivity or spontaneous mutability if deleted. However, the absence of these phenotypes does not contradict its likely role as a positive regulator of dNTP levels.
authors.affiliation: Department of Cell Biology and Anatomy, University of North Texas Health Science Center, Fort Worth, Texas 76107, U.S.A.
authors.forename: Eunmi
authors.initials: E
authors.lastname: Kim
authors.affiliation: Department of Cell Biology and Anatomy, University of North Texas Health Science Center, Fort Worth, Texas 76107, U.S.A.
authors.forename: Wolfram
authors.initials: W
authors.lastname: Siede
keywords: Checkpoints; DNA Damage Tolerance; DNA Repair; Mutagenesis; Yeast; dNTP Pools