Gene Rv3357 (yefM, relB3)
in Mycobacterium tuberculosis H37Rv
General annotation
Type | CDS |
Function | Function unknown |
Product | Antitoxin RelJ |
Comments | Rv3357, (MTV004.14), len: 91 aa. RelJ, antitoxin, part of toxin-antitoxin (TA) operon with Rv3358 (See Cherny et al., 2004; Pandey and Gerdes, 2005), highly similar to other hypothetical proteins e.g. Q9Z4V7|YU1E_STRCO (alias CAC37261|SCBAC17D6.02) ORFU1E (belongs to the PHD/YEFM family) from Streptomyces coelicolor (87 aa), FASTA scores: opt: 344, E(): 1.9e-17, (62.05% identity in 87 aa overlap); P46147|YEFM_ECOLI|B2017 from Escherichia coli strain K12 (83 aa), FASTA scores: opt: 215, E(): 1.6e-08, (50.0% identity in 72 aa overlap); BAB58570|SAV2408 from Staphylococcus aureus subsp. aureus Mu50 (83 aa), FASTA scores: opt: 161, E(): 8.8e-05, (39.95% identity in 77 aa overlap); Q9Z5W8 putative PHD protein from Francisella novicid (85 aa), FASTA scores: opt: 143, E(): 0.0016, (28.9% identity in 83 aa overlap); etc. Also similar to Rv1247c|MTV006.19c (89 aa) (36.9% identity in 84 aa overlap). Seems to belong to the PHD/YEFM family. |
Functional category | Virulence, detoxification, adaptation |
Proteomics | 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). |
Operon | Rv3357 and Rv3358 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 | 3770773 | 3771048 | + |
Genomic sequence
Feature type
Upstream flanking region (bp)
Downstream flanking region (bp)
Update
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv3357|relJ MSISASEARQRLFPLIEQVNTDHQPVRITSRAGDAVLMSADDYDAWQETVYLLRSPENARRLMEAVARDKAGHSAFTKSVDELREMAGGEE
Bibliography
- Sassetti CM et al. [2003]. Genes required for mycobacterial growth defined by high density mutagenesis. Mutant
- Cherny I et al. [2004]. The YefM antitoxin defines a family of natively unfolded proteins: implications as a novel antibacterial target. Product
- Pandey DP et al. [2005]. Toxin-antitoxin loci are highly abundant in free-living but lost from host-associated prokaryotes. Homology
- Kumar P et al. [2008]. Crystal structure of Mycobacterium tuberculosis YefM antitoxin reveals that it is not an intrinsically unstructured protein. Structure
- 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
- 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
- Gupta A [2009]. Killing activity and rescue function of genome-wide toxin-antitoxin loci of Mycobacterium tuberculosis. Function
- Singh R et al. [2010]. The three RelE homologs of Mycobacterium tuberculosis have individual, drug-specific effects on bacterial antibiotic tolerance. Function
- 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