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Thiol reductive stress induces cellulose-anchored biofilm formation in Mycobacterium tuberculosis

Author

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  • Abhishek Trivedi

    (Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh 160036, India)

  • Parminder Singh Mavi

    (Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh 160036, India)

  • Deepak Bhatt

    (Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh 160036, India)

  • Ashwani Kumar

    (Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh 160036, India)

Abstract

Mycobacterium tuberculosis (Mtb) forms biofilms harbouring antibiotic-tolerant bacilli in vitro, but the factors that induce biofilm formation and the nature of the extracellular material that holds the cells together are poorly understood. Here we show that intracellular thiol reductive stress (TRS) induces formation of Mtb biofilms in vitro, which harbour drug-tolerant but metabolically active bacteria with unchanged levels of ATP/ADP, NAD+/NADH and NADP+/NADPH. The development of these biofilms requires DNA, RNA and protein synthesis. Transcriptional analysis suggests that Mtb modulates only ∼7% of its genes for survival in biofilms. In addition to proteins, lipids and DNA, the extracellular material in these biofilms is primarily composed of polysaccharides, with cellulose being a key component. Our results contribute to a better understanding of the mechanisms underlying Mtb biofilm formation, although the clinical relevance of Mtb biofilms in human tuberculosis remains unclear.

Suggested Citation

  • Abhishek Trivedi & Parminder Singh Mavi & Deepak Bhatt & Ashwani Kumar, 2016. "Thiol reductive stress induces cellulose-anchored biofilm formation in Mycobacterium tuberculosis," Nature Communications, Nature, vol. 7(1), pages 1-15, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11392
    DOI: 10.1038/ncomms11392
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