ATP-dependent chromatin-remodeling complexes in DNA double-strand break repair: remodeling, pairing and (re)pairing.
The genomic integrity of a eukaryotic cell is challenged by over 10,000 chromosomal lesions per day. Therefore the cell has evolved efficient mechanisms to recognize, signal, and repair DNA breaks. Defects in any of these steps can lead to chromosomal aberrations and cancers. As these lesions must be repaired in the context of chromatin, both chromatin-modifying and nucleosome-remodeling enzymes have been implicated in DNA damage repair. We reported recently that the RSC and Swi/Snf ATP-dependent chromatin-remodeling complexes are involved in DSB repair specifically by homologous recombination. Here we discuss how such enzymes might be recruited to DNA breaks, why so many remodelers are recruited to sites of DSBs, and a possible functional connection between RSC's roles in sister chromatid cohesion and DSB repair.
Huang
Jian
J
Department of Oncological Science, Mount Sinai School of Medicine, New York, New York 10029, USA.
Liang
Bing
B
Qiu
Jiajing
J
Laurent
Brehon C
BC
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D002843:Chromatin / Q000235:genetics / Q000378:metabolism*; D042002:Chromatin Assembly and Disassembly; D023902:Chromosome Pairing; D004249:DNA Damage; D004260:DNA Repair; D046912:Multiprotein Complexes / Q000378:metabolism
D002843:Chromatin; D046912:Multiprotein Complexes; D000255:Adenosine Triphosphate; D000251:Adenosine Triphosphatases