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Journal of Bacteriology, July 2006, p. 5145-5152, Vol. 188, No. 14
0021-9193/06/$08.00+0 doi:10.1128/JB.00367-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Christine A. Miller,1
Christopher J. Moore,1
Yukio Shirako,2
Masahiko Kobayashi,3 and
Stanley N. Cohen1,4*
Departments of Genetics,1 Medicine, School of Medicine, Stanford University, Stanford, California 94305-5120,4 Asian Natural Environmental Science Center,2 Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan3
Received 14 March 2006/ Accepted 28 April 2006
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.
Present address: Department of Life Science, Chung-Ang University, Seoul 156-756, Korea.
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