Abstract
Toxin/antitoxin (TA) systems are the means by which bacterial cells become persistent; that is, those cells that are tolerant to multiple environmental stresses such as antibiotics by becoming metabolically dormant. These persister cells are responsible for recalcitrant infections. Once toxins are activated by the inactivation of antitoxins (e.g., stress‐triggered Lon degradation of the antitoxin), many toxins reduce metabolism by inhibiting translation (e.g., cleaving mRNA, reducing ATP). The MqsR/MqsA TA system of Escherichia coli cleaves mRNA to help the cell withstand oxidative and bile acid stress. Here, we investigated the role of secondary structure and 5′ mRNA processing on MqsR degradation of mRNA and found that MqsR cleaves only single‐stranded RNA at 5′‐GCU sites and that MqsR is equally active against RNA with 5′‐triphosphate, 5′‐monophosphate, and 5′‐hydroxyl groups.
Highlights
Persister cells, those cells that are tolerant to antibiotics by becoming metabolically dormant, are one of the main causes of recurring infections (Fauvart et al 2011)
Persister cells become dormant through the action of toxin/antitoxin (TA) systems (Keren et al 2004; Harrison et al 2009; Dörr et al 2010; Kim and Wood 2010; Luidalepp et al 2011; Tripathi et al 2014), and TA systems are ubiquitous in prokaryotes (Goeders and Van Melderen 2014)
Secondary structure has a profound impact on the ability of MqsR to degrade mRNA
Summary
Those cells that are tolerant to antibiotics by becoming metabolically dormant, are one of the main causes of recurring infections (Fauvart et al 2011). Toxin MqsR Cleaves mRNA With Various 5′ Ends or RNA (Wang and Wood 2011). In type III TA systems, the RNA antitoxin binds the toxin protein to inhibit it (e.g., ToxN/ToxI as the first member) (Fineran et al 2009). Production of YafQ increases the persistence of biofilm cells 10,000 fold, and its deletion decreases persisence about 2400-fold (Harrison et al 2009) Another type II TA toxin, MazF, induces growth arrest that results in up to a 700- fold increase in persistence compared to a mazF deletion strain (Tripathi et al 2014). Deletion of MqsR/ MqsA was shown to reduce persistence (Kim and Wood 2010), and protein engineering of MqsR to make a more toxic toxin revealed paradoxically that persister cells form more readily when bacteria are less fit (Hong et al 2012). We found that MqsR cleaves primarily ssRNA and that MqsR cleaves ssRNA irrespective of its 5′-ppp, 5′-p, or 5′-OH group
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
