Nagahama Hideki, Oshima Taku, Mori Hirotada, Matsumoto Kouji, Hara Hiroshi
Department of Biochemistry and Molecular Biology, Course in Life Science, Graduate School of Science and Engineering, Saitama University, Saitama 338-8570, Japan.
J Gen Appl Microbiol. 2007 Apr;53(2):143-51. doi: 10.2323/jgam.53.143.
An Escherichia coli pgsA null mutant deficient in acidic phospholipids shows a thermosensitive cell lysis phenotype because of activation of the Rcs phosphorelay signal transduction system. We conducted a DNA microarray analysis with special attention to the genes affected by growth temperature in the mutant deficient in acidic phospholipids. Among the genes identified as highly expressed at high temperature in the pgsA null mutant, the osmB gene was shown to be dependent on the Rcs system for the high expression by dot blot hybridization. Induction of the cloned osmB in the pgsA null mutant caused the thermosensitive defect even in the absence of the Rcs system. Although the deletion of osmB did not suppress the thermosensitivity in the presence of the Rcs system, indicating a multifactorial nature of the deleterious effect of the Rcs activation, we suggest that the osmB hyperexpression is one of the causes of the Rcs-dependent lysis phenotype of the pgsA null mutant.
一种缺乏酸性磷脂的大肠杆菌pgsA基因敲除突变体表现出温度敏感型细胞裂解表型，这是由于Rcs磷酸化信号转导系统被激活所致。我们进行了DNA微阵列分析，特别关注了在缺乏酸性磷脂的突变体中受生长温度影响的基因。在被鉴定为在pgsA基因敲除突变体中高温下高表达的基因中，通过斑点杂交表明osmB基因的高表达依赖于Rcs系统。在pgsA基因敲除突变体中克隆的osmB的诱导即使在没有Rcs系统的情况下也会导致温度敏感缺陷。尽管在存在Rcs系统的情况下osmB的缺失并没有抑制温度敏感性，这表明Rcs激活的有害作用具有多因素性质，但我们认为osmB的过度表达是pgsA基因敲除突变体Rcs依赖性裂解表型的原因之一。
