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dc.contributor.authorRedon, Christophe
dc.contributor.authorPilch, Duane R.
dc.contributor.authorRogakou, Emmy P.
dc.contributor.authorOrr, Ann H.
dc.contributor.authorLowndes, Noel F.
dc.contributor.authorBonner, William M.
dc.date.accessioned2018-08-24T08:26:16Z
dc.date.available2018-08-24T08:26:16Z
dc.date.issued2003-06-06
dc.identifier.citationRedon, Christophe; Pilch, Duane R. Rogakou, Emmy P.; Orr, Ann H.; Lowndes, Noel F.; Bonner, William M. (2003). Yeast histone 2a serine 129 is essential for the efficient repair of checkpoint-blind dna damage. EMBO Reports 4 (7), 678-684
dc.identifier.issn1469-221X,1469-3178
dc.identifier.urihttp://hdl.handle.net/10379/9808
dc.description.abstractCells maintain genomic stability by the coordination of DNA-damage repair and cell-cycle checkpoint control. In replicating cells, DNA damage usually activates intra-S-phase checkpoint controls, which are characterized by delayed S-phase progression and increased Rad53 phosphorylation. We show that in budding yeast, the intra-S-phase checkpoint controls, although functional, are not activated by the topoisomerase I inhibitor camptothecin (CPT). In a CPT-hypersensitive mutant strain that lacks the histone 2A (H2A) phosphatidylinositol-3-OH kinase (PI(3) K) motif at Ser 129 (h2a-s129a), the hypersensitivity was found to result from a failure to process full-length chromosomal DNA molecules during ongoing replication. H2A Ser 129 is not epistatic to the RAD24 and RAD9 checkpoint genes, suggesting a non-checkpoint role for the H2A PI(3) K site. These results suggest that H2A Ser 129 is an essential component for the efficient repair of DNA double-stranded breaks (DSBs) during replication in yeast, particularly of those DSBs that do not induce the intra-S-phase checkpoint.
dc.publisherWiley-Blackwell
dc.relation.ispartofEMBO Reports
dc.subjectdouble-strand breaks
dc.subjectcell-cycle
dc.subjecttopoisomerase-i
dc.subjectreplication
dc.subjecth2ax
dc.subjectpathway
dc.subjectrad53
dc.subjectatm
dc.titleYeast histone 2a serine 129 is essential for the efficient repair of checkpoint-blind dna damage
dc.typeArticle
dc.identifier.doi10.1038/sj.embor.embor871
dc.local.publishedsourcehttp://embor.embopress.org/content/embor/4/7/678.full.pdf
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