Gene Rv1938
in Mycobacterium tuberculosis H37Rv
General annotation
| Type | CDS |
| Function | This enzyme acts on epoxides (alkene oxides, oxiranes) and arene oxides. Plays a role in xenobiotic metabolism by degrading potential toxic epoxides. Also determines steady-state levels of physiological mediators. |
| Product | Probable epoxide hydrolase EphB (epoxide hydratase) |
| Comments | Rv1938, (MTCY09F9.26c), len: 356 aa. Probable ephB, epoxide hydrolase (see citation below), similar to many e.g. G1109600 ATSEH (321 aa), FASTA scores: opt: 442, E(): 1.2e-21 (33.1% identity in 356 aa overlap); etc. Also similar to many other M. tuberculosis hypothetical epoxide hydrolases e.g. Rv3617, Rv3670, Rv0134, etc. |
| Functional category | Virulence, detoxification, adaptation |
| Proteomics | Identified by mass spectrometry in M. tuberculosis H37Rv-infected guinea pig lungs at 90 days but not 30 days (See Kruh et al., 2010). Identified by mass spectrometry in the culture filtrate of M. tuberculosis H37Rv but not the membrane protein fraction or whole cell lysates (See de Souza et al., 2011). |
| Mutant | Non-essential gene for in vitro growth of H37Rv in a MtbYM rich medium, by Himar1 transposon mutagenesis (see Minato et al. 2019). Non-essential gene for in vitro growth of H37Rv, by analysis of saturated Himar1 transposon libraries (see DeJesus et al. 2017). Non essential gene by Himar1 transposon mutagenesis in H37Rv strain (see Sassetti et al., 2003). Non-essential gene for in vitro growth of H37Rv, by Himar1 transposon mutagenesis (See Griffin et al., 2011). M. tuberculosis Erdman Rv1936-Rv1941 mutant is more susceptible to ROS-generating compounds; shows reduced growth and persistence in C57BL/6 and iNOS-/- mice but not Phox -/- mice; pathology in infected C57BL/6 mice is reduced; mutant shows growth defect in activated J774A.1 murine, human peripheral blood monocyte-derived, and mouse bone marrow-derived macrophages (BMDM), and BMDM from Phox -/- and iNOS -/- mice (See Cirillo et al., 2009). Check for mutants available at TARGET website |
Coordinates
| Type | Start | End | Orientation |
|---|---|---|---|
| CDS | 2191027 | 2192097 | + |
Genomic sequence
Feature type
Upstream flanking region (bp)
Downstream flanking region (bp)
Update
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv1938|ephB
VSQVHRILNCRGTRIHAVADSPPDQQGPLVVLLHGFPESWYSWRHQIPALAGAGYRVVAIDQRGYGRSSKYRVQKAYRIKELVGDVVGVLDSYGAEQAFVVGHDWGAPVAWTFAWLHPDRCAGVVGISVPFAGRGVIGLPGSPFGERRPSDYHLELAGPGRVWYQDYFAVQDGIITEIEEDLRGWLLGLTYTVSGEGMMAATKAAVDAGVDLESMDPIDVIRAGPLCMAEGARLKDAFVYPETMPAWFTEADLDFYTGEFERSGFGGPLSFYHNIDNDWHDLADQQGKPLTPPALFIGGQYDVGTIWGAQAIERAHEVMPNYRGTHMIADVGHWIQQEAPEETNRLLLDFLGGLRP
Bibliography
- Tekaia F et al. [1999]. Analysis of the proteome of Mycobacterium tuberculosis in silico. Secondary
- Sassetti CM et al. [2003]. Genes required for mycobacterial growth defined by high density mutagenesis. Mutant
- Biswal BK et al. [2008]. The molecular structure of epoxide hydrolase B from Mycobacterium tuberculosis and its complex with a urea-based inhibitor. Biochemistry Structure
- Cirillo SL et al. [2009]. Protection of Mycobacterium tuberculosis from reactive oxygen species conferred by the mel2 locus impacts persistence and dissemination. Mutant
- de la Paz Santangelo M et al. [2009]. Mce3R, a TetR-type transcriptional repressor, controls the expression of a regulon involved in lipid metabolism in Mycobacterium tuberculosis. Regulon
- Kruh NA et al. [2010]. Portrait of a pathogen: the Mycobacterium tuberculosis proteome in vivo. Proteomics
- Griffin JE et al. [2011]. High-resolution phenotypic profiling defines genes essential for mycobacterial growth and cholesterol catabolism. Mutant
- de Souza GA et al. [2011]. Bacterial proteins with cleaved or uncleaved signal peptides of the general secretory pathway. Proteomics
- DeJesus MA et al. [2017]. Comprehensive Essentiality Analysis of the Mycobacterium tuberculosis Genome via Saturating Transposon Mutagenesis. Mutant
- Minato Y et al. [2019]. Genomewide Assessment of Mycobacterium tuberculosis Conditionally Essential Metabolic Pathways. Mutant
