Learn B A, Grafstrom R H
Department of Microbiology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
J Bacteriol. 1989 Dec;171(12):6473-81. doi: 10.1128/jb.171.12.6473-6481.1989.
The methyl-directed DNA repair efficiency of a series of M13mp9 frameshift heteroduplexes 1, 2, or 3 unpaired bases was determined by using an in vitro DNA mismatch repair assay. Repair of hemimethylated frameshift heteroduplexes in vitro was directed to the unmethylated strand; was dependent on MutH, MutL, and MutS; and was equally efficient on base insertions and deletions. However, fully methylated frameshift heteroduplexes were resistant to repair, while totally unmethylated substrates were repaired with no strand bias. Hemimethylated 1-, 2-, or 3-base insertion and deletion heteroduplexes were repaired by the methyl-directed mismatch repair pathway as efficiently as the G.T mismatch. These results are consistent with earlier in vivo studies and demonstrate the involvement of methyl-directed DNA repair in the efficient prevention of frameshift mutations.
通过体外DNA错配修复试验，测定了一系列具有1个、2个或3个未配对碱基的M13mp9移码异源双链体的甲基定向DNA修复效率。体外半甲基化移码异源双链体的修复作用于未甲基化链；依赖于MutH、MutL和MutS；并且对碱基插入和缺失的修复效率相同。然而，完全甲基化的移码异源双链体对修复具有抗性，而完全未甲基化的底物在修复时没有链偏向性。半甲基化的1个、2个或3个碱基插入和缺失异源双链体通过甲基定向错配修复途径修复的效率与G.T错配相同。这些结果与早期的体内研究一致，并证明甲基定向DNA修复参与了对移码突变的有效预防。
