Gene Rv1916 (icl2b)
in Mycobacterium tuberculosis H37Rv
General annotation
Type | CDS |
Function | Involved in glyoxylate bypass, an alternative to the tricarboxylic acid cycle [catalytic activity: isocitrate = succinate + glyoxylate]. |
Product | Probable isocitrate lyase AceAb [second part] (isocitrase) (isocitratase) (Icl) |
Comments | Rv1916, (MTCY180.02c), len: 398 aa. Probable aceAb, isocitrate lyase (see citations below). Highly similar to the C-terminus of ACEA_MYCLE|P46831 isocitrate lyase from Mycobacterium leprae (606 aa), FASTA results: opt: 1635, E(): 0, (86.3% identity in 278 aa overlap). Although this ORF and the upstream ORF representing the N-terminal half of aceA could be joined by a frameshift no error is apparent in the cosmid, or in a seqencing read from the genome of H37Rv. As this ORF has a RBS and transcriptional start immediately following the stop of the upstream ORF, it is possible that they are expressed as two separate modules. In Mycobacterium tuberculosis strain CDC1551, aceA exists as a single gene, MT1966: the corresponding protein has been purified experimentally and seems have an active isocitrate lyase activity (see Honer et al., 1999). For Mycobacterium tuberculosis strain H37Rv, immunoblot assay didn't detect AceAa or AceAb products (see Honer et al., 1999) but mRNA of AceAa|Rv1915 has been detected (see Betts et al., 2002); so AceAb|Rv1916 could be a pseudogene. Icl2 has 2-methyl-isocitrate lyase (MCL) activity in M. tuberculosis Erdman (See Munoz-Elias et al., 2006). |
Functional category | Intermediary metabolism and respiration |
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 for in vitro growth of H37Rv, by Himar1 transposon mutagenesis (See Griffin et al., 2011). M. tuberculosis Erdman icl1 icl2 mutant is unable to grow on fatty acids, in mice, in macrophages (See Munoz-Elias et al., 2005). Check for mutants available at TARGET website |
Coordinates
Type | Start | End | Orientation |
---|---|---|---|
CDS | 2161566 | 2162762 | + |
Genomic sequence
Feature type
Upstream flanking region (bp)
Downstream flanking region (bp)
Update
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv1916|aceAb MTYGEAVADVLEFGQSEGEPIGMAPEEWRAFAARASLHAARAKAKELGADPPWDCELAKTPEGYYQIRGGIPYAIAKSLAAAPFADILWMETKTADLADARQFAEAIHAEFPDQMLAYNLSPSFNWDTTGMTDEEMRRFPEELGKMGFVFNFITYGGHQIDGVAAEEFATALRQDGMLALARLQRKMRLVESPYRTPQTLVGGPRSDAALAASSGRTATTKAMGKGSTQHQHLVQTEVPRKLLEEWLAMWSGHYQLKDKLRVQLRPQRAGSEVLELGIHGESDDKLANVIFQPIQDRRGRTILLVRDQNTFGAELRQKRLMTLIHLWLVHRFKAQAVHYVTPTDDNLYQTSKMKSHGIFTEVNQEVGEIIVAEVNHPRIAELLTPDRVALRKLITKEA
Bibliography
- Honer zu Bentrup K, Miczak A, Swenson DL and Russell DG [1999]. Characterization of activity and expression of isocitrate lyase in Mycobacterium avium and Mycobacterium tuberculosis. Product Biochemistry Function
- McKinney JD et al. [2000]. Persistence of Mycobacterium tuberculosis in macrophages and mice requires the glyoxylate shunt enzyme isocitrate lyase. Mutant
- Betts JC et al. [2002]. Evaluation of a nutrient starvation model of Mycobacterium tuberculosis persistence by gene and protein expression profiling. Transcriptome
- Muñoz-Elías EJ et al. [2005]. Mycobacterium tuberculosis isocitrate lyases 1 and 2 are jointly required for in vivo growth and virulence. Mutant
- Munoz-Elias EJ, Upton AM, Cherian J and McKinney JD [2006]. Role of the methylcitrate cycle in Mycobacterium tuberculosis metabolism, intracellular growth, and virulence. Function
- Griffin JE et al. [2011]. High-resolution phenotypic profiling defines genes essential for mycobacterial growth and cholesterol catabolism. Mutant
- 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