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Activation of the rcs signal transduction system is responsible for the thermosensitive growth defect of an Escherichia coli mutant lacking phosphatidylglycerol and cardiolipin
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Saitama University, Graduate School of Science and Engineering
雑誌名
Journal of bacteriology
巻
186
号
19
発行年
2004
年月次
2004
出版者名
American Society for Microbiology
DOI
info:doi/10.1128/JB.186.19.6526-6535.2004
抄録
Lethal effect of the Escherichia coli pgsA null mutation which causes a complete lack of the major acidic phospholipids, phosphatidylglycerol and cardiolipin, is alleviated by the lack of the major outer membrane lipoprotein encoded by the lpp gene, but the lpp pgsA strain shows a thermosensitive growth defect. By transposon mutagenesis we found that the hermosensitivity was suppressed by disruption of the rcsC, rcsF, and yojN genes that code for sensor kinase, accessory positive factor, and phosphotransmitter, respectively, of the Rcs phosphorelay signal transduction system initially identified as regulating the capsular polysaccharide synthesis genes (cps). Disruption of the rcsB gene coding for the response regulator of the system also suppressed the thermosensitivity, whereas disruption of cpsE did not. By monitoring the expression of a cpsB′-lac fusion we showed the Rcs system was activated in the pgsA mutant and reversed to a wild-type level by the rcs mutations. These results indicate that the envelope stress due to acidic phospholipid deficiency activates the Rcs phosphorelay system and thereby causes the thermosensitive growth defect independently of the activation of capsule synthesis.
Activation of the rcs signal transduction system is responsible for the thermosensitive growth defect of an Escherichia coli mutant lacking phosphatidylglycerol and cardiolipin
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