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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.

frontiers in microbiology

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