Kim Mandy, Huang Tiffany, Miller Jeffrey H
Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, California 90095, USA.
J Bacteriol. 2003 Aug;185(15):4626-9. doi: 10.1128/JB.185.15.4626-4629.2003.
We show that the MutY protein competes with the MutS-dependent mismatch repair system to process at least some A. C mispairs in vivo, converting them to G. C pairs. In the presence of an increased dCTP pool resulting from the loss of nucleotide diphosphate kinase, the frequency of A. T-->G. C transitions at a hot spot in the rpoB gene is 30-fold lower in a MutY-deficient derivative than in the wild type.
我们发现,MutY蛋白在体内与MutS依赖的错配修复系统竞争,以处理至少一些A·C错配,将它们转化为G·C对。在因核苷酸二磷酸激酶缺失导致dCTP池增加的情况下,rpoB基因热点处A·T→G·C转换的频率在MutY缺陷衍生物中比野生型低30倍。