Journal
JOURNAL OF CELL BIOLOGY
Volume 178, Issue 2, Pages 209-218Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200612031
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Funding
- Intramural NIH HHS Funding Source: Medline
- NIGMS NIH HHS [R37 GM020056, R01 GM061766-07, R01 GM061766, GM61799, GM20056, R01 GM061766-06, R01 GM061766-08, R01 GM020056] Funding Source: Medline
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Double-strand break (DSB) damage in yeast and mammalian cells induces the rapid ATM (ataxia telanglectasia mutated)/ATR (ataxia telangiectasia and Rad3 related)-dependent phosphorylation of histone H2AX (gamma-H2AX). In budding yeast, a single endonuclease-induced DSB triggers gamma-H2AX modification of 50 kb on either side of the DSB. The extent of gamma-H2AX spreading does not depend on the chromosomal sequences. DNA resection after DSB formation causes the slow, progressive loss of gamma-H2AX from single-stranded DNA and, after several hours, the Mecl (ATR)-dependent spreading of gamma-H2AX to more distant regions. Heterochromatic sequences are only weakly modified upon insertion of a 3-kb silent HMR locus into a gamma-H2AX-covered region. The presence of heterochromatin does not stop the phosphorylation of chromatin more distant from the DSB. In mouse embryo fibroblasts, gamma-H2AX distribution shows that gamma-H2AX foci increase in size as chromatin becomes more accessible. In yeast, we see a high level of constitutive gamma-H2AX in telomere regions in the absence of any exogenous DNA damage, suggesting that yeast chromosome ends are transiently detected as DSBs.
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