Overexpression Delays and Entry into Log-Phase and Increases Pathogenicity in Mice.

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