Type II toxin/antitoxin MqsR/MqsA controls type V toxin/antitoxin GhoT/GhoS

Xiaoxue Wang, Dana M. Lord, Seok Hoon Hong, Wolfgang Peti, Michael J. Benedik, Rebecca Page, Thomas K. Wood

Research output: Contribution to journalArticlepeer-review

80 Scopus citations


Toxin endoribonucleases of toxin/antitoxin (TA) systems regulate protein production by selectively degrading mRNAs but have never been shown to control other TA systems. Here we demonstrate that toxin MqsR of the MqsR/MqsA system enriches toxin ghoT mRNAin vivo and in vitro, since this transcript lacks the primary MqsR cleavage site 5′-GCU. GhoT is a membrane toxin that causes the ghost cell phenotype, and is part of a type V TA system with antitoxin GhoS that cleaves specifically ghoT mRNA. Introduction of MqsR primary 5′-GCU cleavage sites into ghoT mRNA reduces ghost cell production and cell death likely due to increased degradation of the altered ghoT mRNA by MqsR. GhoT also prevents cell elongation upon the addition of low levels of ampicillin. Therefore, during stress, antitoxin GhoS mRNA is degraded by toxin MqsR allowing ghoT mRNA translation to yield another free toxin that forms ghost cells and increases persistence. Hence, we show that GhoT/GhoS is the first TA system regulated by another TA system.

Original languageEnglish (US)
Pages (from-to)1734-1744
Number of pages11
JournalEnvironmental microbiology
Issue number6
StatePublished - Jun 2013

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Ecology, Evolution, Behavior and Systematics


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