Progressive structural transitions within Mu transpositional complexes.
Progressive structural transitions within Mu transpositional complexes.
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Mu 转位复合物内的渐进结构转变。
DOI：
10.1016/s1097-2765(02)00796-7
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发表时间：
2003
期刊：
影响因子：
16
通讯作者：
Mizuuchi,Kiyoshi
中科院分区：
文献类型：
--
作者：
Yanagihara,Katsuhiko;Mizuuchi,Kiyoshi
Mu转座体的组装依赖于噬菌体基因组末端附近的MuA转座酶的特异性结合位点。MuA也接触末端核苷酸，但仅在转座体组装时，并且末端核苷酸的碱基特异性识别对于组装是至关重要的。我们表明，Mu末端缺乏终端5 bp可以形成转座体，而较长的DNA底物与突变的终端核苷酸不能。突变的影响可以通过Mu末端附近的碱基错配来抑制。侧翼链的缺失或末端核苷酸的突变对切割和链转移反应具有不同的影响。这些结果表明，末端核苷酸通过影响活性位点周围的构象变化来控制转座体的组装和活化。
Assembly of the Mu transpososome is dependent on specific binding sites for the MuA transposase near the ends of the phage genome. MuA also contacts terminal nucleotides but only upon transpososome assembly, and base-specific recognition of the terminal nucleotides is critical for assembly. We show that Mu ends lacking the terminal 5 bp can form transpososomes, while longer DNA substrates with mutated terminal nucleotides cannot. The impact of the mutations can be suppressed by base mismatches near the end of Mu. Deletion of the flanking strands or mutation of the terminal nucleotides has differential effects on the cleavage and strand transfer reactions. These results show that the terminal nucleotides control the assembly and activation of transpososomes by influencing conformational changes around the active site.