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Type II toxin/antitoxin MqsR / MqsA controls type V toxin/antitoxin GhoT / GhoS
Author(s) -
Wang Xiaoxue,
Lord Dana M.,
Hong Seok Hoon,
Peti Wolfgang,
Benedik Michael J.,
Page Rebecca,
Wood Thomas K.
Publication year - 2013
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.12063
Subject(s) - antitoxin , toxin , biology , messenger rna , microbiology and biotechnology , biochemistry , gene
Summary 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 mRNA in 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.