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Mol. Cell. Biol., Dec 1997, 6868-6875, Vol 17, No. 12
JM Murray, HD Lindsay, CA Munday and AM Carr
The cellular responses to DNA damage are complex and include direct DNA
repair pathways that remove the damage and indirect damage responses which
allow cells to survive DNA damage that has not been, or cannot be, removed.
We have identified the gene mutated in the rad12.502 strain as a
Schizosaccharomyces pombe recQ homolog. The same gene (designated rqh1) is
also mutated in the hus2.22 mutant. We show that Rqhl is involved in a DNA
damage survival mechanism which prevents cell death when UV-induced DNA
damage cannot be removed. This pathway also requires the correct
functioning of the recombination machinery and the six checkpoint rad gene
products plus the Cdsl kinase. Our data suggest that Rqh1 operates during S
phase as part of a mechanism which prevents DNA damage causing cell
lethality. This process may involve the bypass of DNA damage sites by the
replication fork. Finally, in contrast with the reported literature, we do
not find that rqh1 (rad12) mutant cells are defective in UV dimer
endonuclease activity.
Copyright © 1997, American Society for Microbiology
Role of Schizosaccharomyces pombe RecQ homolog, recombination, and checkpoint genes in UV damage tolerance
School of Biological Sciences, Sussex University, Falmer, Brighton, United Kingdom. j.m.murray@sussex.ac.uk
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