Gene Rv1247c (relB1)
in Mycobacterium tuberculosis H37Rv
General annotation
| Type | CDS |
| Function | Function unknown |
| Product | Antitoxin RelB |
| Comments | Rv1247c, (MTV006.19c), len: 89 aa. RelB, antitoxin, part of toxin-antitoxin (TA) operon with Rv1246c (See Pandey and Gerdes, 2005), some similarity to hypothetical proteins including Mycobacterium tuberculosis proteins Rv2865|MTV003.11 (93 aa), FASTA scores: opt: 249, E(): 5.4e-13, (44.2% identity in 86 aa overlap); Rv0268|Z86089|P95225 (169 aa) opt: 125, E(): 0.0089, (41.8% identity in 55 aa overlap); etc. and Escherichia coli AE000293|ECAE0002933 (92 aa), FASTA scores: opt: 127, E(): 0.0038, (29.3% identity in 82 aa overlap). |
| Functional category | Virulence, detoxification, adaptation |
| Proteomics | Identified by mass spectrometry in Triton X-114 extracts of M. tuberculosis H37Rv (See Malen 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). Translational start site supported by proteomics data (See de Souza et al., 2011) (See Kelkar et al., 2011). |
| Operon | Rv1247c and Rv1246c are co-transcribed, by RT-PCR (See Korch et al., 2009). |
| 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). Check for mutants available at TARGET website |
Coordinates
| Type | Start | End | Orientation |
|---|---|---|---|
| CDS | 1388975 | 1389244 | - |
Genomic sequence
Feature type
Upstream flanking region (bp)
Downstream flanking region (bp)
Update
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv1247c|relB
MAVVPLGEVRNRLSEYVAEVELTHERITITRHGHPAAVLISADDLASIEETLEVLRTPGASEAIREGLADVAAGRFVSNDEIRNRYTAR
Bibliography
- Sassetti CM et al. [2003]. Genes required for mycobacterial growth defined by high density mutagenesis. Mutant
- Pandey DP et al. [2005]. Toxin-antitoxin loci are highly abundant in free-living but lost from host-associated prokaryotes. Homology
- Ramage HR, Connolly LE and Cox JS [2009]. Comprehensive functional analysis of Mycobacterium tuberculosis toxin-antitoxin systems: implications for pathogenesis, stress responses, and evolution. Function
- Korch SB et al. [2009]. Three Mycobacterium tuberculosis Rel toxin-antitoxin modules inhibit mycobacterial growth and are expressed in infected human macrophages. Function Operon Product
- Gupta A [2009]. Killing activity and rescue function of genome-wide toxin-antitoxin loci of Mycobacterium tuberculosis. Function
- Målen H et al. [2010]. Definition of novel cell envelope associated proteins in Triton X-114 extracts of Mycobacterium tuberculosis H37Rv. Proteomics
- Singh R et al. [2010]. The three RelE homologs of Mycobacterium tuberculosis have individual, drug-specific effects on bacterial antibiotic tolerance. Function
- Kelkar DS et al. [2011]. Proteogenomic analysis of Mycobacterium tuberculosis by high resolution mass spectrometry. Proteomics Sequence
- de Souza GA et al. [2011]. Bacterial proteins with cleaved or uncleaved signal peptides of the general secretory pathway. 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]. Proteogenomic analysis of polymorphisms and gene annotation divergences in prokaryotes using a clustered mass spectrometry-friendly database. Proteomics Sequence
- 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
