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Toxin-Antitoxin Systems Influence Biofilm and Persister Cell Formation and the General Stress Response

Xiaoxue Wang, Thomas K. Wood
Xiaoxue Wang
1Department of Chemical Engineering, Texas A&M University, College Station, Texas 77843-3122
2Key Laboratory of Marine Bio-Resource Sustainable Utilization, the South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou 510301, People's Republic of China
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Thomas K. Wood
1Department of Chemical Engineering, Texas A&M University, College Station, Texas 77843-3122
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  • For correspondence: Thomas.Wood@chemail.tamu.edu
DOI: 10.1128/AEM.05068-11
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    Fig. 1.

    Type II toxin-antitoxin systems. Type II TA systems are typically transcribed in the same operon with the antitoxin gene preceding the toxin gene (although there are exceptions, such as mqsRA). Transcription of the two genes is generally autoregulated by the toxin-antitoxin complex. Proteases Lon, ClpAP, and ClpXP usually degrade labile protein antitoxins and liberate the toxin. Activated toxins function as endoribonucleases or gyrase inhibitors.

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    Fig. 2.

    Schematic of how toxicity is mediated by mRNA interferases MqsR, MazF, YafQ, and ChpB. Toxin-antitoxin systems are induced by various environmental stresses (indicated by lightning bolts) (Table 1) which serve to induce proteases such as Lon that degrade antitoxins. Upon degradation of the antitoxin, the free toxin cleaves most cellular mRNAs in a sequence-specific manner. This leads to reduced production of large proteins (encoded by mRNAs with cleavage sites shown in black) and an enrichment of small proteins (encoded by mRNAs that lack cleavage sites and shown in orange for MazF, blue for MqsR, green for ChpB, and purple for YafQ) that are death proteins or stress proteins (which help the cell cope with the stress). Cellular mRNAs that contain cleavage sites for each toxin but remain uncleaved are marked with an accessory protein (in brown); these mRNAs may also be protected by secondary structure. The roles of YafQ and ChpB in determining the fate of the cells need to be investigated further.

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    Summary of stress conditions that induce toxin-antitoxin systems

    Stress conditionInduced TA system(s) (reference[s])
    BiofilmMqsRA (60), YoeB/YefM (60)
    Amino acid starvationYafNO (16), HigBA (16), MqsRA (16)
    Oxidative stress (H2O2)MqsRA (38)
    Ampicillin (100 μg/ml)MqsRA (41, 67)
    Chloramphenicol (30 μg/ml)YafNO (16), HigBA (16), MqsRA (16)
    Mitomycin C or SOS responseYafNO (16), YafQ/DinJ (59), TisB/IstR-1 (19), SymE/SymR (35)
    Kanamycin (5 μg/ml)MqsRA (41), YoeB/YefM (41), RelEB (41), HigBA (41), MazFE (41)
    Ciprofloxacin (0.1 μg/ml)TisB/IstR-1 (19)
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Toxin-Antitoxin Systems Influence Biofilm and Persister Cell Formation and the General Stress Response
Xiaoxue Wang, Thomas K. Wood
Applied and Environmental Microbiology Aug 2011, 77 (16) 5577-5583; DOI: 10.1128/AEM.05068-11

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Toxin-Antitoxin Systems Influence Biofilm and Persister Cell Formation and the General Stress Response
Xiaoxue Wang, Thomas K. Wood
Applied and Environmental Microbiology Aug 2011, 77 (16) 5577-5583; DOI: 10.1128/AEM.05068-11
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