Asymmetries generated by transcription-coupled repair in enterobacterial genes

Asymmetries generated by transcription-coupled repair in enterobacterial genes
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DOI:
10.1126/science.272.5258.107
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发表时间:
1996-04-05
期刊:
影响因子:
56.9
通讯作者:
Ochman, H
Ochman, H
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Francino, MP;Chao, L;Ochman, H

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虽然某些复制错误在DNA的每条互补链上以不同的频率发生,但仍不清楚这种偏差是否在染色体复制过程中普遍存在,足以影响序列进化。在这里,检查了肠细菌中的核苷酸替换,在前导链和滞后链之间没有检测到突变率的差异,但是在比较编码链和非编码链时,在编码链上观察到过量的C->T变化。这种不对称性最好用非编码链上的转录偶联修复来解释。虽然绝大多数突变被认为是由复制过程中的自发错误引起的,但这一结果表明DNA损伤是野生突变的重要来源。
Although certain replication errors occur at different frequencies on each of the complementary strands of DNA, it remains unclear whether this bias is prevalent enough during chromosome replication to affect sequence evolution. Here, nucleotide substitutions in enteric bacteria were examined, and no difference in mutation rates was detected between the leading and lagging strands, but in comparing the coding and noncoding strands, an excess of C-->T changes was observed on the coding strand. This asymmetry is best explained by transcription-coupled repair on the noncoding strand. Although the vast majority of mutations are thought to arise from spontaneous errors during replication, this result implicates DNA damage as a substantial source of mutations in the wild.