RNase E maintenance of proper FtsZ/FtsA ratio required for nonfilamentous growth of Escherichia coli cells but not for colony-forming abilityopen access
- Authors
- Tamura, Masaru; Lee, Kangseok; Miller, Christine A.; Moore, Christopher J.; Shirako, Yukio; Kobayashi, Masahiko; Cohen, Stanley N.
- Issue Date
- Jul-2006
- Publisher
- American Society for Microbiology
- Citation
- Journal of Bacteriology, v.188, no.14, pp 5145 - 5152
- Pages
- 8
- Journal Title
- Journal of Bacteriology
- Volume
- 188
- Number
- 14
- Start Page
- 5145
- End Page
- 5152
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/25564
- DOI
- 10.1128/JB.00367-06
- ISSN
- 0021-9193
1098-5530
- Abstract
- 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. Bouché, 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. Copyright © 2006, American Society for Microbiology. All Rights Reserved.
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