This Article Full Text (PDF) Other Versions of this Article: JB.00773-07v1 189/22/8044    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Samaluru, H. Articles by Reddy, M. Search for Related Content PubMed PubMed Citation Articles by Samaluru, H. Articles by Reddy, M.

 Previous Article  |  Next Article 

J. Bacteriol. doi:10.1128/JB.00773-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Role of SufI (FtsP) in cell division of Escherichia coli: evidence for its involvement in stabilization of the division assembly

Centre for Cellular and Molecular Biology, Hyderabad 500007

^* To whom correspondence should be addressed. Email: manjula{at}ccmb.res.in.

	Abstract

The function of SufI, a well-studied substrate of TatABC translocase in Escherichia coli, is not known. It was earlier implicated in cell division, based on the finding that multiple copies of sufI suppressed the mutant phenotypes of ftsI (ftsI23) that encodes a divisomal transpeptidase. Recently, sufI was identified both as a multicopy suppressor and a synthetic lethal of ftsEX that codes for a division-specific putative ABC-transporter. In this study, we show that sufI is essential for the viability of E. coli subjected to various forms of stress including oxidative stress and DNA damage. sufI mutant also exhibits sulA-independent filamentation indicating its role in cell division. The phenotypes of the sufI mutant are suppressed by factors that stabilize the FtsZ ring assembly such as increased expression of cell division proteins FtsQAZ or FtsN, or presence of the gain-of-function ftsA* (FtsA R286W) mutation, suggesting that SufI is a divisomal protein required during stress conditions. In support of this, multicopy sufI suppressed the division defects of mutants carrying ftsA12, ftsQ1 or ftsK44 alleles but not ftsZ84. Most of the division-defective mutants, in particular, those carrying ftsEX or ftsI23 alleles exhibited sensitivity to oxidative stress or DNA damage, and this sensitivity was also abolished by multiple copies of SufI. All these data suggest that SufI is a division component involved in protecting or stabilizing the divisomal assembly in conditions of stress. Since sufI fulfils the requirements to be designated as an fts gene, we propose that it be renamed ftsP.

This article has been cited by other articles:

• Robichon, C., King, G. F., Goehring, N. W., Beckwith, J. (2008). Artificial Septal Targeting of Bacillus subtilis Cell Division Proteins in Escherichia coli: an Interspecies Approach to the Study of Protein-Protein Interactions in Multiprotein Complexes. J. Bacteriol. 190: 6048-6059 [Abstract] [Full Text]