期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2003
卷号：100
期号：26
页码：15959-15964
DOI：10.1073/pnas.2536607100
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The mechanosensitive (MS) channels MscS and MscL are essential for the survival of hypoosmotic shock by Escherichia coli cells. We demonstrate that MscS and MscL are induced by osmotic stress and by entry into stationary phase. Reduced levels of MS proteins and reduced expression of mscL- and mscS-LacZ fusions in an rpoS mutant strain suggested that the RNA polymerase holoenzyme containing {sigma}S is responsible, at least in part, for regulating production of MS channel proteins. Consistent with the model that the effect of {sigma}S is direct, the MscS and MscL promoters both use RNA polymerase containing {sigma}S in vitro. Conversely, clpP or rssB mutations, which cause enhanced levels of {sigma}S, show increased MS channel protein synthesis. RpoS null mutants are sensitive to hypoosmotic shock upon entry into stationary phase. These data suggest that MscS and MscL are components of the RpoS regulon and play an important role in ensuring structural integrity in stationary phase bacteria.
