GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
PMID:7644534
| Citation |
Collins, DM, Kawakami, RP, de Lisle, GW, Pascopella, L, Bloom, BR and Jacobs, WR Jr (1995) Mutation of the principal sigma factor causes loss of virulence in a strain of the Mycobacterium tuberculosis complex. Proc. Natl. Acad. Sci. U.S.A. 92:8036-40 |
|---|---|
| Abstract |
Tuberculosis continues to be responsible for the deaths of millions of people, yet the virulence factors of the causative pathogens remain unknown. Genetic complementation experiments with strains of the Mycobacterium tuberculosis complex have identified a gene from a virulent strain that restores virulence to an attenuated strain. The gene, designated rpoV, has a high degree of homology with principal transcription or sigma factors from other bacteria, particularly Mycobacterium smegmatis and Streptomyces griseus. The homologous rpoV gene of the attenuated strain has a point mutation causing an arginine-->histidine change in a domain known to interact with promoters. To our knowledge, association of loss of bacterial virulence with a mutation in the principal sigma factor has not been previously reported. The results indicate either that tuberculosis organisms have an alternative principal sigma factor that promotes virulence genes or, more probably, that this particular mutant principal sigma factor is unable to promote expression of one or more genes required for virulence. Study of genes and proteins differentially regulated by the mutant transcription factor should facilitate identification of further virulence factors. |
| Links | |
| Keywords |
Amino Acid Sequence; Animals; Base Sequence; Cloning, Molecular; Cosmids; Genes, Bacterial; Genetic Complementation Test; Guinea Pigs; Molecular Sequence Data; Mycobacterium/genetics; Mycobacterium bovis/genetics; Mycobacterium bovis/pathogenicity; Mycobacterium tuberculosis/genetics; Mycobacterium tuberculosis/pathogenicity; Open Reading Frames; Recombination, Genetic; Sequence Deletion; Sequence Homology, Nucleic Acid; Sigma Factor/genetics; Sigma Factor/physiology; Spleen/microbiology; Spleen/pathology; Streptomyces griseus/genetics; Tuberculosis/physiopathology; Virulence/physiology |
| edit table |
Significance
Annotations
| Gene product | Qualifier | GO Term | Evidence Code | with/from | Aspect | Extension | Notes | Status |
|---|---|---|---|---|---|---|---|---|
| GO:0016987: sigma factor activity |
ECO:0000315: |
F |
Figure 1 shows (A) Randomly selected clones from the pool inoculated into guinea pigs and (B) Representative clones recovered from spleen lesions. Figure 2 show Spleens from guinea pigs inoculated with M. bovis ATCC35721 (A) M. bovis ATCC35721 containing the integrating vector and (B) integrating vector with an insert that included rpoV (sigma factor) from M. bovis. Mutation that causes M. bovis ATCC35721 to become attenuated encoded a putative principal sigma factor that was designated rpoV. |
complete | ||||
| GO:0016987: sigma factor activity |
ECO:0000315: |
F |
Figure 2 show Spleens from guinea pigs inoculated with M. bovis ATCC35721 (A) M. bovis ATCC35721 containing the integrating vector and (B) integrating vector with an insert that included rpoV (sigma factor) from M. bovis. Mutation that causes M. bovis ATCC35721 to become attenuated encoded a putative principal sigma factor that was designated rpoV. |
complete | ||||
See also
References
See Help:References for how to manage references in GONUTS.
