| Antitoxin MqsA helps mediate the bacterial general stress response. | |
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MedLine Citation:
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PMID: 21516113 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Although it is well recognized that bacteria respond to environmental stress through global networks, the mechanism by which stress is relayed to the interior of the cell is poorly understood. Here we show that enigmatic toxin-antitoxin systems are vital in mediating the environmental stress response. Specifically, the antitoxin MqsA represses rpoS, which encodes the master regulator of stress. Repression of rpoS by MqsA reduces the concentration of the internal messenger 3,5-cyclic diguanylic acid, leading to increased motility and decreased biofilm formation. Furthermore, the repression of rpoS by MqsA decreases oxidative stress resistance via catalase activity. Upon oxidative stress, MqsA is rapidly degraded by Lon protease, resulting in induction of rpoS. Hence, we show that external stress alters gene regulation controlled by toxin-antitoxin systems, such that the degradation of antitoxins during stress leads to a switch from the planktonic state (high motility) to the biofilm state (low motility). |
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Authors:
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Xiaoxue Wang; Younghoon Kim; Seok Hoon Hong; Qun Ma; Breann L Brown; Mingming Pu; Aaron M Tarone; Michael J Benedik; Wolfgang Peti; Rebecca Page; Thomas K Wood |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S. Date: 2011-04-24 |
Journal Detail:
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Title: Nature chemical biology Volume: 7 ISSN: 1552-4469 ISO Abbreviation: Nat. Chem. Biol. Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-05-18 Completed Date: 2011-07-26 Revised Date: 2011-12-21 |
Medline Journal Info:
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Nlm Unique ID: 101231976 Medline TA: Nat Chem Biol Country: United States |
Other Details:
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Languages: eng Pagination: 359-66 Citation Subset: IM |
Affiliation:
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Department of Chemical Engineering, Texas A&M University, College Station, Texas, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antitoxins
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physiology* Bacterial Proteins / biosynthesis, genetics Biofilms DNA-Binding Proteins / physiology* Escherichia coli Proteins / physiology* Gene Expression Regulation, Bacterial / physiology Plankton Protease La / metabolism Sigma Factor / biosynthesis, genetics Stress, Physiological* / genetics |
| Grant Support | |
ID/Acronym/Agency:
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R01 EB003872-05/EB/NIBIB NIH HHS; R01 GM089999-03/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antitoxins; 0/Bacterial Proteins; 0/DNA-Binding Proteins; 0/Escherichia coli Proteins; 0/MqsA protein, E coli; 0/Sigma Factor; 0/sigma factor KatF protein, Bacteria; EC 3.4.21.53/Protease La |
| Comments/Corrections | |
Comment In:
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Nat Chem Biol. 2011 Jun;7(6):345-7
[PMID:
21587255
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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