Heterochromatin is refractory to gamma-H2AX modification in yeast and mammals Export

@article{citeulike:2148300, abstract = {Double-strand break (DSB) damage in yeast and mammalian cells induces the rapid ATM (ataxia telangiectasia 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 Mec1 (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. 10.1083/jcb.200612031}, author = {Kim, Jung-Ae and Kruhlak, Michael and Dotiwala, Farokh and Nussenzweig, Andre and Haber, James E.}, citeulike-article-id = {2148300}, citeulike-linkout-0 = {http://dx.doi.org/10.1083/jcb.200612031}, citeulike-linkout-1 = {http://www.jcb.org/cgi/content/abstract/178/2/209}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/17635934}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=17635934}, day = {16}, doi = {10.1083/jcb.200612031}, journal = {J. Cell Biol.}, keywords = {chromatin, chromatin-remodeling-modification, dna-damage, h2a, h2ax, histone, phosphorylation, yeast}, month = {July}, number = {2}, pages = {209--218}, posted-at = {2007-12-19 20:35:32}, priority = {2}, title = {Heterochromatin is refractory to {gamma}-H2AX modification in yeast and mammals}, url = {http://dx.doi.org/10.1083/jcb.200612031}, volume = {178}, year = {2007} }

TY - JOUR ID - citeulike:2148300 L3 - citeulike-article-id:2148300 N2 - Double-strand break (DSB) damage in yeast and mammalian cells induces the rapid ATM (ataxia telangiectasia 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 Mec1 (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. 10.1083/jcb.200612031 IS - 2 JF - J. Cell Biol. EP - 218 TI - Heterochromatin is refractory to {gamma}-H2AX modification in yeast and mammals VL - 178 SP - 209 KW - chromatin KW - chromatin-remodeling-modification KW - dna-damage KW - h2a KW - h2ax KW - histone KW - phosphorylation KW - yeast AU - Kim, Jung-Ae AU - Kruhlak, Michael AU - Dotiwala, Farokh AU - Nussenzweig, Andre AU - Haber, James PY - 2007/07/16/ UR - http://dx.doi.org/10.1083/jcb.200612031 ER -