期刊
NUCLEIC ACIDS RESEARCH
卷 46, 期 12, 页码 6152-6165出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gky481
关键词
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资金
- Grant for International Health Research from the Ministry of Health, Labour and Welfare of Japan [29A1028]
- JSPS KAKENHI [18K06190]
- Council for Science, Technology and Innovation (CSTI) ImPACT Program
- Grants-in-Aid for Scientific Research [18K06190] Funding Source: KAKEN
Mismatch repair (MMR) systems based on MutS eliminate mismatches originating from replication errors. Despite extensive conservation of mutS homologues throughout the three domains of life, Actinobacteria and some archaea do not have genes homologous to mutS. Here, we report that EndoMS/NucS of Corynebacterium glutamicum is the mismatch-specific endonuclease that functions cooperatively with a sliding clamp. EndoMS/NucS function in MMR was fully dependent on physical interaction between EndoMS/NucS and sliding clamp. A combination of endoMS/nucS gene disruption and a mutation in dnaE, which reduced the fidelity of DNA polymerase, increased the mutation rate synergistically and confirmed the participation of EndoMS in replication error correction. EndoMS specifically cleaved G/T, G/G and T/T mismatches in vitro, and such substrate specificity was consistent with the mutation spectrum observed in genome-wide analyses. The observed substrate specificity of EndoMS, together with the effects of endoMS gene disruption, led us to speculate that the MMR system, regardless of the types of proteins in the system, evolved to address asymmetrically occurring replication errors in which G/T mismatches occur much more frequently than C/A mismatches.
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