AUTHOR=Liu Dan , Hao Kewei , Wang Wenjie , Peng Chao , Dai Yue , Jin Ruiliang , Xu Wenxi , He Lei , Wang Hongyan , Wang Honghai , Zhang Lu , Wang Qingzhong 

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

JOURNAL=Frontiers in Microbiology

VOLUME=8

YEAR=2017

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2017.02231

DOI=10.3389/fmicb.2017.02231

ISSN=1664-302X

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