MSMEG_5684 down-regulation in Mycobacterium smegmatis affects its permeability, survival under stress and persistence

Keshari, Deepa; Singh, Kumar Sachin; Sharma, Rolee; Yadav, Shailendra; Singh, S. N.

doi:10.1016/j.tube.2017.01.004

Cited by 5 publications

(1 citation statement)

References 33 publications

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“…The non-replicating persistent form of M. tuberculosis aids the escape of the pathogen from the host defense mechanisms and provides additional advantage to the bacilli as regards the effect of standard anti-TB drugs. This process results in the long term survival of the bacteria for several decades ( Voskuil et al, 2003 ; Keshari et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Rv2629 Overexpression Delays Mycobacterium smegmatis and Mycobacteria tuberculosis Entry into Log-Phase and Increases Pathogenicity of Mycobacterium smegmatis in Mice

et al. 2017

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Objective: The aim of the present study was to explore the potential biological role of Rv2629 in Mycobacterium smegmatis and Mycobacterium tuberculosis.Methods: Recombinant wild type and mutant Rv2629 strains were constructed. Rv2629 expression was evaluated by real-time PCR and western blot. Microarray and interaction network analyses were used to identify the gene interactions associated with wild type and mutant Rv2629. Bacterial growth was assessed in Balb/c mice infected with wild type and mutant Rv2629 strains using CFU assay and histological analysis of the organs.Results: Overexpression of Rv2629 could delay the entry of the Mycobacterium tuberculosis cells into the log-phase, while Rv2629 decreased the number of ribosomes and the expression of uridylate kinase in Mycobacterium smegmatis. The Gene Ontology (GO) and pathway analysis indicated that 122 genes correlated with wild type Rv2629, whereas the Rv2629 mutation led to decrease in the ribosome production, oxidative phosphorylation, and virulence in Mycobacterium tuberculosis. Overexpression of Rv2629 slightly enhanced the drug resistance of Mycobacterium smegmatis to antibiotics, and increased its survival and pathogenicity in Balb/c mice.Conclusion: It is suggested that Rv2629 is involved in the survival of the clinical drug-resistant strain via bacterial growth repression and bacterial persistence induction.

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Section: Introductionmentioning

confidence: 99%