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virulence, detoxification, adaptation
information pathways
cell wall and cell processes
stable RNAs
insertion seqs and phages
intermediary metabolism and respiration
regulatory proteins
conserved hypotheticals
lipid metabolism
General annotation
FunctionProbably involved in biosynthesis of phthiocerol dimycocerosate (PDIM)
ProductProbable thioesterase TesA
CommentsRv2928, (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 categoryLipid metabolism
ProteomicsIdentified 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).
TranscriptomicsmRNA 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).
MutantNon-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
Genomic sequence
Feature type Upstream flanking region (bp) Downstream flanking region (bp) Update
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv2928|tesA