Affiliation:
1. Department of Molecular Biology and Genetics, Graduate Program in Cell and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205
Abstract
ABSTRACT
Yeast cells can survive in the absence of telomerase RNA,
TLC1
, by recombination-mediated telomere elongation. Two types of survivors, type I and type II, can be distinguished by their characteristic telomere patterns.
RAD52
is essential for the generation of both types of survivors. Deletion of both
RAD50
and
RAD51
produces a phenotype similar to that produced by deletion of
RAD52
. Here we examined the effects of the
RAD50
and the
RAD51
epistasis groups as well as the
RAD52
homologue,
RAD59
, on the types of survivors generated in the absence of telomerase.
rad59
mutations completely abolished the ability to generate type II survivors, while
rad50
mutations decreased the growth viability of type II survivors but did not completely eliminate their appearance. Mutations in
RAD51, RAD54
, and
RAD57
had the converse affect: they eliminated the ability of cells to generate type I survivors in a
tlc1
strain. The triple mutant,
tlc1 rad51 rad59
, was not able to generate survivors. Thus either type I or type II recombination pathways can allow cells to survive in the absence of telomerase; however, elimination of both pathways in a telomerase mutant leads to the inability to elongate telomeres and ultimately cell death.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
245 articles.
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