期刊
ANNUAL REVIEW OF BIOCHEMISTRY
卷 73, 期 -, 页码 589-615出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev.biochem.73.012803.092453
关键词
FEN1; structure-specific endonuclease; DNA replication; DNA long-patch base excision repair; genomic stability
资金
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM024441] Funding Source: NIH RePORTER
- NIGMS NIH HHS [GM24441] Funding Source: Medline
One strand of cellular DNA is generated as RNA-initiated discontinuous segments called Okazaki fragments that later are joined. The RNA terminated region is displaced into a 5' single-stranded flap, which is removed by the structure-specific flap endonuclease 1 (FEN1), leaving a nick for ligation. Similarly, in long-patch base excision repair, a damaged nucleotide is displaced into a flap and removed by FEN1. FEN1 is a genome stabilization factor that prevents flaps from equilibrating into structures that lead to duplications and deletions. As an endonuclease, FEN1 enters the flap from the 5' end and then tracks to cleave the flap base. Cleavage is oriented by the formation of a double flap. Analyses of FEN1 crystal structures suggest mechanisms for tracking and cleavage. Some flaps can form self-annealed and template bubble structures that interfere with FEN1. FEN1 interacts with other nucleases and helicases that allow it to act efficiently on structured flaps. Genetic and biochemical analyses continue to reveal many roles of FEN1.
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