RcsA-dependent and -independent growth defects caused by the activated Rcs phosphorelay system in the Escherichia coli pgsA null mutant

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  • Nagahama Hideki
    Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University
  • Sakamoto Yutaka
    Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University
  • Matsumoto Kouji
    Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University
  • Hara Hiroshi
    Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University

Abstract

In the Escherichia coli pgsA null mutant, which lacks the major acidic phospholipids, the Rcs phosphorelay signal transduction system is activated, causing thermosensitive growth. The mutant grows poorly at 37°C and lyses at 42°C. We showed that the poor growth at 37°C was corrected by disruption of the rcsA gene, which codes for a coregulator protein that interacts with the RcsB response regulator of the phosphorelay system. However, mutant cells still lysed when incubated at 42°C even in the absence of RcsA. We conclude that the activated Rcs phosphorelay in the pgsA null mutant has both RcsA-dependent and -independent growth inhibitory effects. Since the Rcs system has been shown to positively regulate the essential cell division genes ftsA and ftsZ independently of RcsA, we measured cellular levels of the FtsZ protein, but found that the growth defect of the mutant at 42°C did not involve a change in the level of this protein.

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