Zavilgelsky G B, Kotova V Yu, Melkina O E, Balabanov V P, Mindlin S Z
Mol Biol (Mosk). 2015 Mar-Apr;49(2):334-41.
Conjugative plasmids and conjugative transposons contain the genes, which products specifically inhibit the type I restriction--modification systems. Here is shown that non-conjugative transposons Tn2l, Tn5053, Tn5045, Tn501, Tn402 partially inhibit the restriction activity of the type I restriction-modification endonuclease EcoKI (R2M2S1) in Escherichia coli cells K12 (the phenomenon of restriction alleviation, RA). Antirestriction activity of the transposons is determined by the MerR and ArdD proteins. Antirestriction activity of transposons is absent in mutants E. coli K12 clpX and clpP and is decreased in mutants E. coli K12 recA, recBC and dnaQ (mutD). Induction of the RA in response to the MerR and ArdD activities is consistent with the production of unmodified target sequences following DNA repair and DNA synthesis associated with recombination repair or replication errors. RA effect is determined by the ClpXP-dependent degradation of the endonuclease activity R subunit of EcoKI (R2M2S1).
接合质粒和接合转座子含有一些基因，其产物能特异性抑制I型限制-修饰系统。本文表明，非接合转座子Tn2l、Tn5053、Tn5045、Tn501、Tn402能部分抑制大肠杆菌K12细胞中I型限制-修饰内切酶EcoKI（R2M2S1）的限制活性（限制缓解现象，RA）。转座子的抗限制活性由MerR和ArdD蛋白决定。在大肠杆菌K12 clpX和clpP突变体中，转座子不存在抗限制活性，而在大肠杆菌K12 recA、recBC和dnaQ（mutD）突变体中，转座子的抗限制活性降低。响应MerR和ArdD活性而诱导的RA与DNA修复和与重组修复或复制错误相关的DNA合成后产生未修饰的靶序列一致。RA效应由ClpXP依赖的EcoKI（R2M2S1）内切酶活性R亚基的降解决定。
