期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 98, 期 15, 页码 8350-8354出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.111007198
关键词
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资金
- NIGMS NIH HHS [GM21422, R37 GM021422, GM42554, R01 GM021422] Funding Source: Medline
DNA polymerase V, composed of a heterotrimer of the DNA damage-inducible UmuC and UmuD(2)' proteins, working in conjunction with RecA, single-stranded DNA (ssDNA)-binding protein (SSB), beta sliding clamp, and gamma clamp loading complex, are responsible for most SOS lesion-targeted mutations in Escherichia coli, by catalyzing translesion synthesis (TLS). DNA polymerase II, the product of the damage-inducible polB (dinA) gene plays a pivotal role in replication-restart, a process that bypasses DNA damage in an error-free manner. Replication-restart takes place almost immediately after the DNA is damaged (approximate to min post-UV irradiation), whereas TLS occurs after pol V is induced approximate to 50 min later. We discuss recent data for pol V-catalyzed TLS and pol II-catalyzed replication-restart. Specific roles during TLS for pol V and each of its accessory factors have been recently determined. Although the precise molecular mechanism of pol II-dependent replication-restart remains to be elucidated, it has recently been shown to operate in conjunction with RecFOR and PriA proteins.
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