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首页> 外文期刊>Journal of Molecular Biology >RNase HII Saves rnhA Mutant Escherichia coli from R-Loop-Associated Chromosomal Fragmentation
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RNase HII Saves rnhA Mutant Escherichia coli from R-Loop-Associated Chromosomal Fragmentation

机译：RNase HII将RNHA突变体大肠杆菌储存来自R环相关的染色体碎片

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The rnhAB mutant Escherichia coli, deficient in two RNase H enzymes that remove both R-loops and incorporated ribonucleotides (rNs) from DNA, grow slowly, suggesting accumulation of rN-containing DNA lesions (R-lesions). We report that the rnhAB mutants have reduced viability, form filaments with abnormal nucleoids, induce SOS, and fragment their chromosome, revealing replication and/or segregation stress. R-loops are known to interfere with replication forks, and sensitivity of the double rnhAB mutants to translation inhibition points to R-loops as precursors for R-lesions. However, the strict specificity of bacterial RNase HII for RNA DNA junctions indicates that R-lesions have rNs integrated into DNA. Indeed, instead of relieving problems of rnhAB mutants, transient inhibition of replication from oriC kills them, suggesting that oriC-initiated replication removes R-loops instead of compounding them to R-lesions. Yet, replication from an R-loop-initiating plasmid origin kills the double rnhAB mutant, revealing generation of R-lesions by R-loop-primed DNA synthesis. These R-lesions could be R-tracts, contiguous runs of 4 RNA nucleotides within DNA strand and the only common substrate between the two bacterial RNase H enzymes. However, a plasmid relaxation test failed to detect R-tracts in DNA of the rnhAB mutants, although it readily detected R-patches (runs of 1-3 rNs). Instead, we detected R-gaps, single-strand gaps containing rNs, in the chromosomal DNA of the rnhAB mutant. Therefore, we propose that RNase H-deficient mutants convert some R-loops into R-tracts, which progress into R-gaps and then to double-strand breaks explaining why R-tracts do not accumulate in RNase H-deficient cells, while double-strand breaks do. (C) 2017 Elsevier Ltd. All rights reserved.
机译：RNHAB突变体大肠杆菌，缺乏两种RNA酶H酶，其除去R-LOOPS并从DNA掺入核糖核苷酸（RNS），缓慢生长，表明含RN的DNA病变（R-病变）的积累。我们报道了rnhab突变体具有降低的活力，形成核心异常的细丝，诱导SOS，并染色染色体，揭示复制和/或分离应激。已知R环会干扰复制叉，并且双RNHAB突变体对翻译抑制点的敏感性作为R损伤的前体。然而，对RNA DNA连接点的细菌RNase HII的严格特异性表明R-病变使RNS集成到DNA中。实际上，而不是缓解RNHAB突变体的问题，瞬态抑制来自ORIC的复制杀死它们，表明ORIC引发的复制去除R圈，而不是将它们混合给R病变。然而，来自R环的激素来源的复制杀死双RNHAB突变体，通过R环诱导的DNA合成揭示R-病变的产生。这些R-病变可以是R型，DNA链中的4个RNA核苷酸的连续循环，并且两种细菌RNase H酶之间的唯一常见底物。然而，质粒弛豫测试未能检测RNHAB突变体的DNA中的R型r型，尽管它容易检测到R型贴剂（延伸1-3 rns）。相反，在RNHAB突变体的染色体DNA中，我们检测到含有RN的R-隙，含有RN的单链间隙。因此，我们提出RNase H缺陷型突变体将一些R循环转化为R-沟，这进入R-THAPS，然后向双链断裂解释为什么R-arracts不会在RNase H缺陷细胞中积累，而双重-strand打破了。 （c）2017 Elsevier Ltd.保留所有权利。

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