Journal
SCIENCE
Volume 297, Issue 5581, Pages 602-606Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1071398
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Funding
- NIGMS NIH HHS [GM25326, R01 GM025326] Funding Source: Medline
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Budding yeast Mec1, homolog of mammalian ATR, is an essential protein that mediates S-phase checkpoint responses and meiotic recombination. Elimination of Mec1 function leads to genomewide fork stalling followed by chromosome breakage. Breaks do not result from stochastic collapse of stalled forks or other incidental lesions; instead, they occur in specific regions of the genome during a G(2) chromosomal transition. Break regions are found to be genetically encoded replication slow zones (RSZs), a newly discovered yeast chromosomal determinant. Thus, Mec1 has important functions in normal S phase and the genome instability of mec1 (and, analogously, ATR(-/-)) mutants stems from defects in these basic roles.
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