首页> 美国卫生研究院文献>Nucleic Acids Research >Statistical evaluation and biological interpretation of non-random abundance in the E. coli K-12 genome of tetra- and pentanucleotide sequences related to VSP DNA mismatch repair.
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Statistical evaluation and biological interpretation of non-random abundance in the E. coli K-12 genome of tetra- and pentanucleotide sequences related to VSP DNA mismatch repair.

机译:与VSP DNA错配修复相关的四核苷酸和五核苷酸序列在大肠杆菌K-12基因组中的非随机丰度的统计评估和生物学解释。

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摘要

The abundance of all tetra- and pentanucleotide sequences is calculated for a set of DNA sequence data comprising 767,393 nucleotides of the E. coli K-12 genome. Observed frequencies are compared to those expected from a Markov chain prediction algorithm. Systematic and extreme non-random representations are found for special sets of sequences. These are interpreted as arising from incorporation of a 2'-deoxyguanosine residue opposite thymidine during replication which, in special sequence contexts, leads to a T/G mismatch that is simultaneously substrate for two competing DNA mismatch repair systems: the mutHLS and the VSP pathway. Processing by the former leads to error correction, by the latter to mutation fixation. The significance of the latter process, as demonstrated here, makes it unlikely that VSP repair has evolved mainly as a mutation avoidance mechanism. It is proposed that in E. coli K-12, VSP repair, together with DNA cytosine methylation, constitutes a mutagenesis/recombination system capable of promoting gene-conversion-like unidirectional transfer of short stretches of DNA sequence.
机译:对于一组包含大肠杆菌K-12基因组的767,393个核苷酸的DNA序列数据,计算了所有四核苷酸和五核苷酸序列的丰度。将观察到的频率与马尔可夫链预测算法预期的频率进行比较。对于特殊的序列集,发现了系统的和极端的非随机表示。这些被解释为是由于在复制过程中与胸苷相对的2'-脱氧鸟苷残基的掺入而引起的,在特殊序列的情况下,T / G错配同时是两个竞争性DNA错配修复系统的底物:mutHLS和VSP途径。前者的处理导致错误纠正,后者的处理导致突变固定。如此处所示,后一个过程的重要性使得VSP修复不太可能主要发展为避免突变机制。提出在大肠杆菌K-12中,VSP修复与DNA胞嘧啶甲基化一起构成了诱变/重组系统,其能够促进短序列DNA序列的基因转化样单向转移。

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