Spontaneous mutations occur near dam recognition sites in a dam- Escherichia coli host.
Spontaneous mutations occur near dam recognition sites in a dam- Escherichia coli host.
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自发突变发生在母体大肠杆菌宿主中的母体识别位点附近。
DOI：
10.1093/genetics/116.3.343
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发表时间：
1987
期刊：
影响因子：
3.3
通讯作者：
Marinus,MG
中科院分区：
文献类型：
--
作者：
Carraway,M;Youderian,P;Marinus,MG
E.coliK12的错配修复系统去除DNA中的错配碱基。如果DNA的任何一条链在5‘-GATC-3’序列中缺少N6-甲基腺嘌呤，则可能发生错配修复。在半甲基化的异源双链中，修复优先发生在未甲基化的链上。如果两条链都完全甲基化，修复就会受到抑制。突变株(DAM-)；在识别5‘-GATC-3’序列(DAM)的腺嘌呤甲基酶中有结肠缺陷，因此错配修复有缺陷，与其他同基因的DAM+宿主相比，显示出更高的自发突变率。我们已经分离并鉴定了91个独立的突变，这些突变是由质粒携带的噬菌体P22抑制基因MNT中的Dam缺陷引起的。这些突变大多是A：T→G：C转换，发生在该基因两个5‘-GATC-3’序列的6个碱基对内。相反，ADAM+宿主的mnt-突变谱由大多数插入的IS元件和不聚集在Dam识别位点附近的缺失组成。这些结果表明，Dam指导的复制后错配修复在体内纠正潜在的转换突变方面发挥了重要作用，并表明与Dam识别位点相关的序列特别容易发生复制或修复错误。
The mismatch repair system ofEscherichia coliK12 removes mispaired bases from DNA. Mismatch repair can occur on either strand of DNA if it lacks N6-methyladenines within 5′-GATC-3′ sequences. In hemimethylated heteroduplexes, repair occurs preferentially on the unmethylated strand. If both strands are fully methylated, repair is inhibited. Mutant (dam-) strains ofE. colidefective in the adenine methylase that recognizes 5′-GATC-3′ sequences (Dam), and therefore defective in mismatch repair, show increased spontaneous mutation rates compared to otherwise isogenicdam+hosts. We have isolated and characterized 91 independent mutations that arise as a consequence of the Dam-defect in a plasmid-borne phage P22 repressor gene,mnt. The majority of these mutations are A:T→G:C transitions that occur within six base pairs of the two 5′-GATC-3′ sequences in themntgene. In contrast, the spectrum ofmnt-mutations in adam+host is comprised of a majority of insertions of IS elements and deletions that do not cluster near Dam recognition sites. These results show that Dam-directed post-replicative mismatch repair plays a significant role in the rectification of potential transition mutationsin vivo, and suggest that sequences associated with Dam recognition sites are particularly prone to replication or repair errors.