Gene Rv3574
in Mycobacterium tuberculosis H37Rv
General annotation
Type | CDS |
Function | Involved in transcriptional mechanism. Predicted to control regulon involved in lipid metabolism |
Product | Transcriptional regulatory protein KstR (probably TetR-family) |
Comments | Rv3574, (MTCY06G11.21), len: 199 aa. Probable kstR, transcriptional regulator TetR family, similar to others e.g. Q9KXK1|SCC53.10 from Streptomyces coelicolor (250 aa) FASTA scores: opt: 492, E(): 4.8e-25, (44.8% identity in 183 aa overlap); Q9RA03|KSTR from Rhodococcus erythropolis (208 aa), FASTA scores: opt: 294, E(): 3.1e-12, (28.9% identity in 187 aa overlap); BAB54261|MLR7895 from Rhizobium loti (Mesorhizobium loti) (193 aa), FASTA scores: opt: 166, E(): 0.00062, (32.05% identity in 78 aa overlap); P17446|BETI_ECOLI|B0313 from Escherichia coli strain K12 (195 aa), FASTA scores: opt: 142, E(): 0.0034, (25. 6% identity in 168 aa overlap); etc. Equivalent to AAK48038 from Mycobacterium tuberculosis strain CDC1551 (243 aa) but shorter 44 aa. Contains possible helix-turn-helix motif from aa 37-58 (+3.70 SD). Possibly belongs to the TetR/AcrR family of transcriptional regulators. |
Functional category | Regulatory proteins |
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). |
Transcriptomics | 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 and CDC1551 strains (see Sassetti et al., 2003 and Lamichhane et al., 2003). Required for growth in C57BL/6J mouse spleen, by transposon site hybridization (TraSH) in H37Rv (See Sassetti and Rubin, 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 | 4016484 | 4017083 | + |
Genomic sequence
Feature type
Upstream flanking region (bp)
Downstream flanking region (bp)
Update
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv3574|kstR VAVLAESELGSEAQRERRKRILDATMAIASKGGYEAVQMRAVADRADVAVGTLYRYFPSKVHLLVSALGREFSRIDAKTDRSAVAGATPFQRLNFMVGKLNRAMQRNPLLTEAMTRAYVFADASAASEVDQVEKLIDSMFARAMANGEPTEDQYHIARVISDVWLSNLLAWLTRRASATDVSKRLDLAVRLLIGDQDSA
Bibliography
- Sassetti CM and Rubin EJ [2003]. Genetic requirements for mycobacterial survival during infection. Mutant
- Sassetti CM et al. [2003]. Genes required for mycobacterial growth defined by high density mutagenesis. Mutant
- Lamichhane G et al. [2003]. A postgenomic method for predicting essential genes at subsaturation levels of mutagenesis: application to Mycobacterium tuberculosis. Mutant
- Talaat AM et al. [2004]. The temporal expression profile of Mycobacterium tuberculosis infection in mice. Transcriptome
- Kendall SL, Withers M, Soffair CN, Moreland NJ, Gurcha S, Sidders B, Frita R, Ten Bokum A, Besra GS, Lott JS and Stoker NG [2007]. A highly conserved transcriptional repressor controls a large regulon involved in lipid degradation in Mycobacterium smegmatis and Mycobacterium tuberculosis. 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