Antitoxin DinJ influences the general stress response through transcript stabilizer CspE

Ying Hu, Michael J. Benedik, Thomas K. Wood

Research output: Contribution to journalArticle

54 Scopus citations

Abstract

Antitoxins are becoming recognized as proteins that regulate more than their own synthesis; for example, we found previously that antitoxin MqsA of the Escherichia coli toxin/antitoxin (TA) pair MqsR/MqsA directly represses the gene encoding the stationary-phase sigma factor RpoS. Here, we investigated the physiological role of antitoxin DinJ of the YafQ/DinJ TA pair and found DinJ also affects the general stress response by decreasing RpoS levels. Corroborating the reduced RpoS levels upon producing DinJ, the RpoS-regulated phenotypes of catalase activity, cell adhesins and cyclic diguanylate decreased while swimming increased. Using a transcriptome search and DNA-binding assays, we determined that the mechanism by which DinJ reduces RpoS is by repressing cspE at the LexA palindrome; cold-shock protein CspE enhances translation of rpoS mRNA. Inactivation of CspE abolishes the ability of DinJ to influence RpoS. Hence, DinJ influences the general stress response indirectly by regulating cspE.

Original languageEnglish (US)
Pages (from-to)669-679
Number of pages11
JournalEnvironmental microbiology
Volume14
Issue number3
DOIs
StatePublished - Mar 1 2012

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Ecology, Evolution, Behavior and Systematics

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