The AraC Family Transcriptional Regulator Rv1931c Plays a Role in the Virulence of Mycobacterium tuberculosis

ABSTRACT A Mycobacterium tuberculosis strain disrupted in the AraC homologue Rv1931c was isolated. The mutant strain exhibited reduced survival both in macrophages and in a mouse infection model, with survival being restored on complementation with the Rv1931c gene. These results suggest that Rv1931c regulates genes important for virulence of M. tuberculosis.

[1]  W. Bishai,et al.  Mycobacterium tuberculosis ECF sigma factor sigC is required for lethality in mice and for the conditional expression of a defined gene set , 2004, Molecular microbiology.

[2]  J. Saldanha,et al.  A two-component signal transduction system with a PAS domain-containing sensor is required for virulence of Mycobacterium tuberculosis in mice. , 2004, Biochemical and biophysical research communications.

[3]  Shruti Jain,et al.  mymA operon of Mycobacterium tuberculosis: its regulation and importance in the cell envelope. , 2003, FEMS microbiology letters.

[4]  B. Sclavi,et al.  Mycobacterium tuberculosis Rv1395 Is a Class III Transcriptional Regulator of the AraC Family Involved in Cytochrome P450 Regulation* , 2003, Journal of Biological Chemistry.

[5]  E. Rubin,et al.  Genes required for mycobacterial growth defined by high density mutagenesis , 2003, Molecular microbiology.

[6]  Tanya Parish,et al.  Deletion of Two-Component Regulatory Systems Increases the Virulence of Mycobacterium tuberculosis , 2003, Infection and Immunity.

[7]  V. Mizrahi,et al.  DNA Alkylation Damage as a Sensor of Nitrosative Stress in Mycobacterium tuberculosis , 2003, Infection and Immunity.

[8]  K. Papavinasasundaram,et al.  DNA damage induction of recA in Mycobacterium tuberculosis independently of RecA and LexA , 2002, Molecular microbiology.

[9]  R. Fleischmann,et al.  Reduced immunopathology and mortality despite tissue persistence in a Mycobacterium tuberculosis mutant lacking alternative σ factor, SigH , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[10]  W. Jacobs,et al.  Mycobacterium tuberculosis WhiB3 interacts with RpoV to affect host survival but is dispensable for in vivo growth , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[11]  V. Deretic,et al.  Mycobacterium tuberculosis signal transduction system required for persistent infections , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[12]  B. Gicquel,et al.  An essential role for phoP in Mycobacterium tuberculosis virulence , 2001, Molecular microbiology.

[13]  T. Dick,et al.  Mycobacterium bovis BCG recADeletion Mutant Shows Increased Susceptibility to DNA-Damaging Agents but Wild-Type Survival in a Mouse Infection Model , 2001, Infection and Immunity.

[14]  J. Rosner,et al.  The AraC transcriptional activators. , 2001, Current opinion in microbiology.

[15]  E. Böttger,et al.  Instability and site-specific excision of integration-proficient mycobacteriophage L5 plasmids: development of stably maintained integrative vectors. , 2001, International journal of medical microbiology : IJMM.

[16]  B. Gicquel,et al.  Identification of a virulence gene cluster of Mycobacterium tuberculosis by signature‐tagged transposon mutagenesis , 1999, Molecular microbiology.

[17]  S. Jain,et al.  Analysis, expression and prevalence of the Mycobacterium tuberculosis homolog of bacterial virulence regulating proteins. , 1999, FEMS microbiology letters.

[18]  A Bairoch,et al.  Arac/XylS family of transcriptional regulators , 1997, Microbiology and molecular biology reviews : MMBR.

[19]  E. Böttger,et al.  rpsL+: a dominant selectable marker for gene replacement in mycobacteria , 1995, Molecular microbiology.