Raposa S, Fox M S
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.
Genetics. 1987 Nov;117(3):381-90. doi: 10.1093/genetics/117.3.381.
We have used artificially constructed heteroallelic heteroduplex molecules of bacteriophage lambda DNA to transfect Escherichia coli, and E. coli mutants deficient in various functions involved in the adenine methylation-directed mismatch repair system, MutL, MutS, MutH, and UvrD (MutU). Analysis of the allele content of single infective centers shows that this repair system often acts on several mismatches, separated by as many as 2000 bp, on one of the strands of a heteroduplex molecule. When the methyl-directed mismatch repair system is disabled by mutH or uvrD mutations, localized mismatch repair becomes prominent. This prominent localized repair that can result in separation of very closely linked markers requires the functions MutL and MutS, is independent of adenine methylation, and appears to reflect another mechanism of mismatch repair. Heterology-containing heteroduplex molecules with a deletion in one strand often escape processing. However, when the heterology includes the stem and loop structure of a transposon, Tn10, the transposon is lost.
我们使用人工构建的噬菌体λDNA异源等位基因异源双链分子转染大肠杆菌,以及参与腺嘌呤甲基化导向错配修复系统、MutL、MutS、MutH和UvrD(MutU)的各种功能缺陷的大肠杆菌突变体。对单个感染中心的等位基因含量分析表明,该修复系统通常作用于异源双链分子一条链上多达2000 bp间隔的多个错配。当甲基导向错配修复系统因mutH或uvrD突变而失活时,局部错配修复变得突出。这种可导致紧密连锁标记分离的突出局部修复需要MutL和MutS功能,独立于腺嘌呤甲基化,似乎反映了错配修复的另一种机制。一条链上有缺失的含异源双链分子通常逃避加工。然而,当异源双链包括转座子Tn10的茎环结构时,转座子会丢失。