Toxin YafQ increases persister cell formation by reducing indole signalling. (8th August 2014)

• Record Type: Journal Article
• Authors: Hu, Ying; Kwan, Brian W.; Osbourne, Devon O.; Benedik, Michael J.; Wood, Thomas K.
• Is Part Of: Environmental microbiology. Volume 17:Number 4(2015:Apr.)
• Page Start: 1275
• Page End: 1285
• Publication Date: 2014-08-08
• Subjects: Microbial ecology -- Periodicals; Environmental Microbiology -- Periodicals; 579.17
• DOI: 10.1111/1462-2920.12567
• Languages: English
• ISSNs: 1462-2912

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>Persister cells survive antibiotic and other environmental stresses by slowing metabolism. Since toxins of toxin/antitoxin (TA) systems have been postulated to be responsible for persister cell formation, we investigated the influence of toxin YafQ of the YafQ/DinJ <italic>E</italic><italic>scherichia coli</italic> TA system on persister cell formation. Under stress, YafQ alters metabolism by cleaving transcripts with in‐frame 5′‐AAA‐G/A‐3′ sites. Production of YafQ increased persister cell formation with multiple antibiotics, and by investigating changes in protein expression, we found that YafQ reduced tryptophanase levels (TnaA mRNA has 16 putative YafQ cleavage sites). Consistently, TnaA mRNA levels were also reduced by YafQ. Tryptophanase is activated in the stationary phase by the stationary‐phase sigma factor RpoS, which was also reduced dramatically upon production of YafQ. Tryptophanase converts tryptophan into indole, and as expected, indole levels were reduced by the production of YafQ. Corroborating the effect of YafQ on persistence, addition of indole reduced persistence. Furthermore, persistence increased upon deleting <italic>tnaA</italic>, and persistence decreased upon adding tryptophan to the medium to increase indole levels. Also, YafQ production had a much smaller effect on persistence in a strain unable to produce indole. Therefore, YafQ increases persistence by reducing indole, and TA systems are related to cell signalling.</p> </abstract>