期刊
ANNUAL REVIEW OF GENETICS, VOL 44
卷 44, 期 -, 页码 113-139出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-genet-051710-150955
关键词
cyclin-dependent kinase; DNA damage response (DDR); DNA repair; phosphorylation; sumoylation; ubiquitylation
资金
- NATIONAL CANCER INSTITUTE [R01CA092276, R03CA092776] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM058015] Funding Source: NIH RePORTER
- NCI NIH HHS [R03 CA092776, R01 CA092276, CA92776] Funding Source: Medline
- NIGMS NIH HHS [GM58015, R01 GM058015] Funding Source: Medline
Homologous recombination (HR) is required for accurate chromosome segregation during the first meiotic division and constitutes a key repair and tolerance pathway for complex DNA damage, including DNA double-strand breaks, interstrand crosslinks, and DNA gaps. In addition, recombination and replication are inextricably linked, as recombination recovers stalled and broken replication forks, enabling the evolution of larger genomes/replicons. Defects in recombination lead to genomic instability and elevated cancer predisposition, demonstrating a clear cellular need for recombination. However, recombination can also lead to genome rearrangements. Unrestrained recombination causes undesired endpoints (translocation, deletion, inversion) and the accumulation of toxic recombination intermediates. Evidently, HR must be carefully regulated to match specific cellular needs. Here, we review the factors and mechanistic stages of recombination that are subject to regulation and suggest that recombination achieves flexibility and robustness by proceeding through metastable, reversible intermediates.
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