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Abstract：
Most, but not all, homologous genetic recombination in bacteria is mediated by the RecA recombinase. The mechanistic origin of RecA-independent recombination has remained enigmatic. Here, we demonstrate that the RarA protein makes a major enzymatic contribution to RecA-independent recombination. In particular, RarA makes substantial contributions to intermolecular recombination and to recombination events involving relatively short (<200 bp) homologous sequences, where RecA-mediated recombination is inefficient. The effects are seen here in plasmid-based recombination assays and in vivo cloning processes. Vestigial levels of recombination remain even when both RecA and RarA are absent. Additional pathways for RecA-independent recombination, possibly mediated by helicases, are suppressed by exonucleases ExoI and RecJ. Translesion DNA polymerases may also contribute. Our results provide additional substance to a previous report of a functional overlap between RecA and RarA.
摘要：
大多数,但不是全部,细菌中的同源基因重组是由RecA重组酶介导的。RecA独立重组的机制起源仍然是神秘的。这里,我们证明RarA蛋白对RecA非依赖性重组具有主要的酶促作用。特别是,RarA对分子间重组和涉及相对较短（<200bp）同源序列的重组事件做出了重大贡献，其中RecA介导的重组效率低下。在基于质粒的重组测定和体内克隆过程中可以看到这种效果。即使RecA和RarA都不存在，重组的残留水平仍然存在。RecA非依赖性重组的其他途径，可能是由解旋酶介导的，被外切核酸酶ExoI和RecJ抑制。转录DNA聚合酶也可能有贡献。我们的结果为先前有关RecA和RarA之间功能重叠的报道提供了其他内容。
