RNase E maintenance of proper FtsZ/FtsA ratio required for nonfilamentous growth of Escherichia coli cells but not for colony-forming ability

RNase E maintenance of proper FtsZ/FtsA ratio required for nonfilamentous growth of Escherichia coli cells but not for colony-forming ability
复制标题

DOI:
10.1128/jb.00367-06
复制
发表时间:
2006-07-01
影响因子:
3.2
通讯作者:
Cohen, Stanley N.
Cohen, Stanley N.
中科院分区:
生物学3区
文献类型:
--
作者:
Tamura, Masaru;Lee, Kangseok;Cohen, Stanley N.

文献摘要

被引文献

相似文献

大肠杆菌的RNase E编码基因的失活或缺失导致细菌细胞在液体培养物中生长为丝状链(K. Goldblum和D. Apirion,J. Bacteriol. 146:128-132,1981)和在固体培养基上丧失集落形成能力(CFA)。RNase E功能障碍也与ftsQAZ转录物的异常加工有关(K. Cam,G.罗马,H. M. Krisch和J. - P. Bouche,Nucleic Acids Res.24:3065-3070,1996),其编码在细胞分裂期间隔膜形成中具有中心作用的蛋白质。我们在这里表明,RNase E调节FtsZ和FtsA蛋白的相对丰度,RNase E耗竭导致FtsZ减少,FtsA增加,从而改变FtsZ/FtsA比率。然而,虽然在一个无效突变细菌中FtsZ水平恢复到正常逆转了表达表型,但它不能恢复CFA。相反,在rne缺失的细菌中过表达相关的RNA酶,RNA酶G,恢复CFA,如先前报道的,而不影响FtsZ丰度。我们的研究结果表明,RNase E活性是维持大肠杆菌中FtsZ和FtsA蛋白的适当细胞比例所必需的。但FtsZ缺陷并不能解释缺乏RNase E的细胞不能存活。
Inactivation or deletion of the RNase E-encoding rne gene of Escherichia coli results in the growth of bacterial cells as filamentous chains in liquid culture (K. Goldblum and D. Apirion, J. Bacteriol. 146:128-132, 1981) and the loss of colony-forming ability (CFA) on solid media. RNase E dysfunction is also associated with abnormal processing of ftsQAZ transcripts (K. Cam, G. Rome, H. M. Krisch, and J.-P. Bouche, Nucleic Acids Res. 24:3065-3070, 1996), which encode proteins having a central role in septum formation during cell division. We show here that RNase E regulates the relative abundances of FtsZ and FtsA proteins and that RNase E depletion results in decreased FtsZ, increased FtsA, and consequently an altered FtsZ/FtsA ratio. However, while restoration of the level of FtsZ to normal in rne null mutant bacteria reverses the filamentation phenotype, it does not restore CFA. Conversely, overexpression of a related RNase, RNase G, in rne-deleted bacteria restores CFA, as previously reported, without affecting FtsZ abundance. Our results demonstrate that RNase E activity is required to maintain a proper cellular ratio of the FtsZ and FtsA proteins in E. coli but that FtsZ deficiency does not account for the nonviability of cells lacking RNase E.