Gene Rv2928
in Mycobacterium tuberculosis H37Rv
General annotation
| Type | CDS |
| Function | Probably involved in biosynthesis of phthiocerol dimycocerosate (PDIM) |
| Product | Probable thioesterase TesA |
| Comments | Rv2928, (MTCY338.17), len: 261 aa. Probable tesA, thioesterase, similar to many e.g. Q9L4W2|NYSE thioesterase involved in synthesis of the polyene antifungal antibiotic nystatin from Streptomyces noursei (see Brautaset et al., 2000) (251 aa). TesA|Rv2928 interacts with PpsE|Rv2935, by bacterial two-hybrid and GST-pulldown assays (See Rao and Ranganathan, 2004). |
| Functional category | Lipid metabolism |
| Proteomics | Identified in the membrane fraction of M. tuberculosis H37Rv using 1D-SDS-PAGE and uLC-MS/MS (See Gu et al., 2003). 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 whole cell lysates of M. tuberculosis H37Rv but not the culture filtrate or membrane protein fraction (See de Souza et al., 2011). |
| Transcriptomics | mRNA identified by DNA microarray analysis and possibly down-regulated by hrcA|Rv2374c (see Stewart et al., 2002). DNA microarrays show increased expression in M. tuberculosis H37Rv in BALB/c mice compared to SCID mice, after 21 days of infection (See Talaat et al., 2004). |
| 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). Essential gene for in vitro growth of H37Rv, by Himar1 transposon mutagenesis (See Griffin et al., 2011). M. tuberculosis H37Rv tesA|Rv2928 transposon mutant does not produce phthiocerol dimycocerosate (PDIM) (See Waddell et al., 2005). M. marinum tesA|MMAR_1778 transposon mutant lacks PDIM A, PDIM B, and PGLs, defect corrected by complemetation; mutant is more susceptible to some antibiotics (partially complemented by tesA expression) but not isoniazid (See Alibaud et al., 2011). M. marinum tesA|MMAR_1778 deletion mutant produces only trace amounts of PDIMs and PGLs, defect corrected by complementation with tesA but not tesA-S92A; mutant is more susceptible to several antibiotics (complemented by tesA expression) but not streptomycin (See Chavadi et al., 2011). Check for mutants available at TARGET website |
Coordinates
| Type | Start | End | Orientation |
|---|---|---|---|
| CDS | 3242198 | 3242983 | + |
Genomic sequence
Feature type
Upstream flanking region (bp)
Downstream flanking region (bp)
Update
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv2928|tesA
MLARHGPRYGGSVNGHSDDSSGDAKQAAPTLYIFPHAGGTAKDYVAFSREFSADVKRIAVQYPGQHDRSGLPPLESIPTLADEIFAMMKPSARIDDPVAFFGHSMGGMLAFEVALRYQSAGHRVLAFFVSACSAPGHIRYKQLQDLSDREMLDLFTRMTGMNPDFFTDDEFFVGALPTLRAVRAIAGYSCPPETKLSCPIYAFIGDKDWIATQDDMDPWRDRTTEEFSIRVFPGDHFYLNDNLPELVSDIEDKTLQWHDRA
Bibliography
- Brautaset T, Sekurova ON, Sletta H, Ellingsen TE, Strtm AR, Valla S and Zotchev SB [2000]. Biosynthesis of the polyene antifungal antibiotic nystatin in Streptomyces noursei ATCC 11455: analysis of the gene cluster and deduction of the biosynthetic pathway. Homolog Secondary
- Stewart GR et al. [2002]. Dissection of the heat-shock response in Mycobacterium tuberculosis using mutants and microarrays. Transcriptome Regulation
- Dahl JL et al. [2003]. The role of RelMtb-mediated adaptation to stationary phase in long-term persistence of Mycobacterium tuberculosis in mice. Regulon
- Sassetti CM et al. [2003]. Genes required for mycobacterial growth defined by high density mutagenesis. Mutant
- Gu S et al. [2003]. Comprehensive proteomic profiling of the membrane constituents of a Mycobacterium tuberculosis strain. Proteomics
- Talaat AM et al. [2004]. The temporal expression profile of Mycobacterium tuberculosis infection in mice. Transcriptome
- Rao A et al. [2004]. Interaction studies on proteins encoded by the phthiocerol dimycocerosate locus of Mycobacterium tuberculosis. Biochemistry
- Waddell SJ, Chung GA, Gibson KJ, Everett MJ, Minnikin DE, Besra GS and Butcher PD [2005]. Inactivation of polyketide synthase and related genes results in the loss of complex lipids in Mycobacterium tuberculosis H37Rv. Mutant Operon
- 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
- [2011]. A Mycobacterium marinum TesA mutant defective for major cell wall-associated lipids is highly attenuated in Dictyostelium discoideum and zebrafish embryos. Function Mutant
- [2011]. Inactivation of tesA reduces cell wall lipid production and increases drug susceptibility in mycobacteria. Function 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
