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E-dependent cell lysis in Escherichia coli: roles of RpoE regulators RseA, RseB and periplasmic folding catalyst PpiD
1 Applied Molecular Bioscience, Graduate School of Medicine, Yamaguchi University, Ube 755-8505, Japan
2 Department of Biological Chemistry, Faculty of Agriculture, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan
3 Division of Medical and Biochemical Microbiology, Research Center Borstel, Parkallee 22, Borstel 23845, Germany
To understand the mechanism of 
E-dependent cell lysis, we examined the consequences of deletion derivatives of rpoE regulators rseA, rseB and rseC on E transcription, on levels of free versus membrane-bound E and on OMP-biogenesis limiting factor(s) that could impact cell lysis. RT-PCR showed that individual nonpolar 
rseA and rseB increased the rpoE expression to varying extents, with pronounced induction in rseA. Significantly the ratio of soluble (free) versus membrane-bound form of RpoE increased in rseA, however without increase of its total amount, unraveling furthermore complexity in RpoE regulation. Significant characteristics of cell lysis, accompanied by a severe reduction in the levels of periplasmic OMP-folding factor (PpiD), were observed in rseA. The cell-lysis phenotype of rseA was suppressed by either rseA or ppiD plasmids, but neither by rseB nor by rseC clones. However, the cell lysis of the wild-type strain was almost completely repressed not only by the rseA clone but also by the rseB clone, suggesting RseB might be limiting in vivo. Thus, increase in the ratio of free E in rseA mutants with a concomitant reduction in PpiD levels can account for E-dependent lysis in concert with a potential role of small RNAs on the lysis process.
* Correspondence: m-yamada{at}yamaguchi-u.ac.jp
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