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学科主题: Microbiology
题名: Type II toxin/antitoxin MqsR/MqsA controls type V toxin/antitoxin GhoT/GhoS
作者: [Wang, Xiaoxue] Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Marine Bioresources Sustainable Utilizat, Guangzhou, Guangdong, Peoples R China ; [Lord, Dana M. ; Peti, Wolfgang] Brown Univ, Dept Mol Pharmacol, Providence, RI 02912 USA ; [Page, Rebecca] Brown Univ, Dept Mol Biol Cell Biol & Biochem, Providence, RI 02912 USA ; [Hong, Seok Hoon ; Wood, Thomas K.] Texas A&M Univ, Dept Chem Engn, College Stn, TX 77843 USA ; [Wood, Thomas K.] Penn State Univ, Dept Chem Engn, University Pk, PA 16802 USA ; [Wood, Thomas K.] Penn State Univ, Dept Biochem & Mol Biol, University Pk, PA 16802 USA
通讯作者: tuw14@psu.edu
刊名: ENVIRONMENTAL MICROBIOLOGY
发表日期: 2013
卷: 15, 期:6, 页:1734-1744
部门归属: LMB
资助者: This work was supported by the NIH (R01 GM089999 to T. W.), the NSF (CAREER award MCB 0952550 to R. P.), the NSFC (31270214 to X. W.) and the 1000-Youth Elite Program from China (to X. W.). We are grateful for the Keio and ASKA strains provided by the Genome Analysis Project in Japan and for the help of Brian Kwan with a persistence assay. T. W. is the Biotechnology Endowed Professor at the Pennsylvania State University.
摘要: 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.
语种: 英语
原文出处: 查看原文
WOS记录号: WOS:000319873300006
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内容类型: 期刊论文
URI标识: http://ir.scsio.ac.cn/handle/344004/11021
Appears in Collections:中科院海洋生物资源可持续利用重点实验室_期刊论文

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[Wang, Xiaoxue] Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Marine Bioresources Sustainable Utilizat, Guangzhou, Guangdong, Peoples R China; [Lord, Dana M.; Peti, Wolfgang] Brown Univ, Dept Mol Pharmacol, Providence, RI 02912 USA; [Page, Rebecca] Brown Univ, Dept Mol Biol Cell Biol & Biochem, Providence, RI 02912 USA; [Hong, Seok Hoon; Wood, Thomas K.] Texas A&M Univ, Dept Chem Engn, College Stn, TX 77843 USA; [Wood, Thomas K.] Penn State Univ, Dept Chem Engn, University Pk, PA 16802 USA; [Wood, Thomas K.] Penn State Univ, Dept Biochem & Mol Biol, University Pk, PA 16802 USA.Type II toxin/antitoxin MqsR/MqsA controls type V toxin/antitoxin GhoT/GhoS,ENVIRONMENTAL MICROBIOLOGY,2013,15(6):1734-1744
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