
RNase E Maintenance of Proper FtsZ/FtsA Ratio Required for Nonfilamentous Growth of Escherichia coli Cells but Not for Colony-Forming Ability
Author(s) -
Masahito Tamura,
Kangseok Lee,
Christine Miller,
Christopher Moore,
Yukio Shirako,
Masahiko Kobayashi,
Stanley N. Cohen
Publication year - 2006
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.00367-06
Subject(s) - ftsz , rnase p , biology , escherichia coli , rnase h , mutant , cell division , microbiology and biotechnology , rnase mrp , genetics , biochemistry , rna , gene , cell
Inactivation or deletion of the RNase E-encodingrne gene ofEscherichia 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 offtsQAZ 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 inrne null mutant bacteria reverses the filamentation phenotype, it does not restore CFA. Conversely, overexpression of a related RNase, RNase G, inrne -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 inE. coli but that FtsZ deficiency does not account for the nonviability of cells lacking RNase E.