噬菌体T4中自发和诱导移码突变的机制。
Mechanisms of spontaneous and induced frameshift mutation in bacteriophage T4.
作者信息
Streisinger G, Owen J
出版信息
Genetics. 1985 Apr;109(4):633-59. doi: 10.1093/genetics/109.4.633.
Abstract
Frequencies of spontaneous and proflavine-induced frameshift mutations increased dramatically as a function of the number of reiterated base pairs at each of two sites in the lysozyme gene of bacteriophage T4. At each site, proflavine induces addition mutations more frequently than deletion mutations. We confirm that the steroidal diamine, irehdiamine A, induces frameshift addition mutations. At sites of reiterated bases, we propose that base pairing is misaligned adjacent to a gap. The misaligned configuration is stabilized by the stacking of mutagen molecules around the extrahelical base, forming a sandwich. Proflavine induces addition mutations efficiently at a site without any reiterated bases. Mutagenesis at such sites may be due to mutagen-induced stuttering of the replication complex.
摘要
在噬菌体T4溶菌酶基因的两个位点上，自发的和原黄素诱导的移码突变频率随着重复碱基对数量的增加而急剧增加。在每个位点，原黄素诱导添加突变的频率高于缺失突变。我们证实甾体二胺irehdiamine A可诱导移码添加突变。在重复碱基位点，我们提出碱基配对在缺口附近会发生错配。错配构型通过诱变剂分子围绕螺旋外碱基的堆积而得以稳定，形成一种夹心结构。原黄素在没有任何重复碱基的位点也能高效诱导添加突变。此类位点的诱变可能是由于诱变剂诱导复制复合物的滑动。
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