Chromosome-wide Rad51 spreading and SUMO-H2A.Z-dependent chromosome fixation in response to a persistent DNA double-strand break. Export

@article{citeulike:4095381, abstract = {DNA double-strand breaks (DSBs) are acutely hazardous for cells, as they can cause genome instability. DSB repair involves the sequential recruitment of repair factors to the DSBs, followed by Rad51-mediated homology probing, DNA synthesis, and ligation. However, little is known about how cells react if no homology is found and DSBs persist. Here, by monitoring a single persistent DNA break, we show that, following DNA resection and RPA recruitment, Rad51 spreads chromosome-wide bidirectionally from the DSB but selectively only on the broken chromosome. Remarkably, the persistent DSB is later fixed to the nuclear periphery in a process that requires Rad51, the histone variant H2A.Z, its SUMO modification, and the DNA-damage checkpoint. Indeed, H2A.Z is deposited close to the break early but transiently and directs DNA resection, single DSB-induced checkpoint activation, and DSB anchoring. Thus, a persistent DSB induces a multifaceted response, which is linked to a specific chromatin mark.}, author = {Kalocsay, M. and Hiller, N. J. and Jentsch, S.}, citeulike-article-id = {4095381}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.molcel.2009.01.016}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19217407}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19217407}, day = {13}, doi = {10.1016/j.molcel.2009.01.016}, issn = {1097-4164}, journal = {Molecular cell}, keywords = {dna-damage, double-strand-break, h2az, rad51}, month = {February}, number = {3}, pages = {335--343}, posted-at = {2009-02-24 20:52:53}, priority = {2}, title = {Chromosome-wide Rad51 spreading and SUMO-H2A.Z-dependent chromosome fixation in response to a persistent DNA double-strand break.}, url = {http://dx.doi.org/10.1016/j.molcel.2009.01.016}, volume = {33}, year = {2009} }

TY - JOUR ID - citeulike:4095381 L3 - citeulike-article-id:4095381 N2 - DNA double-strand breaks (DSBs) are acutely hazardous for cells, as they can cause genome instability. DSB repair involves the sequential recruitment of repair factors to the DSBs, followed by Rad51-mediated homology probing, DNA synthesis, and ligation. However, little is known about how cells react if no homology is found and DSBs persist. Here, by monitoring a single persistent DNA break, we show that, following DNA resection and RPA recruitment, Rad51 spreads chromosome-wide bidirectionally from the DSB but selectively only on the broken chromosome. Remarkably, the persistent DSB is later fixed to the nuclear periphery in a process that requires Rad51, the histone variant H2A.Z, its SUMO modification, and the DNA-damage checkpoint. Indeed, H2A.Z is deposited close to the break early but transiently and directs DNA resection, single DSB-induced checkpoint activation, and DSB anchoring. Thus, a persistent DSB induces a multifaceted response, which is linked to a specific chromatin mark. IS - 3 JF - Molecular cell SN - 1097-4164 EP - 343 TI - Chromosome-wide Rad51 spreading and SUMO-H2A.Z-dependent chromosome fixation in response to a persistent DNA double-strand break. VL - 33 SP - 335 KW - dna-damage KW - double-strand-break KW - h2az KW - rad51 AU - Kalocsay, M AU - Hiller, NJ AU - Jentsch, S PY - 2009/02/13/ UR - http://dx.doi.org/10.1016/j.molcel.2009.01.016 ER -