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virulence, detoxification, adaptation
information pathways
cell wall and cell processes
stable RNAs
insertion seqs and phages
PE/PPE
intermediary metabolism and respiration
unknown
regulatory proteins
conserved hypotheticals
lipid metabolism
pseudogenes
General annotation
TypeCDS
FunctionRepair of alkylated guanine in DNA by stoichiometrically transferring the alkyl group at the O-6 position to a cysteine residue in the enzyme. This is a suicide reaction: the enzyme is irreversibly inactivated [catalytic activity: DNA (containing 6-O-methylguanine) + [protein]-L-cysteine = DNA (without 6-O-methylguanine) + protein S-methyl-L-cysteine.]
ProductMethylated-DNA--protein-cysteine methyltransferase Ogt (6-O-methylguanine-DNA methyltransferase) (O-6-methylguanine-DNA-alkyltransferase)
CommentsRv1316c, (MTCY130.01c), len: 165 aa. Ogt, methylated-dna--protein-cysteine methytransferase (see citation below), similar to many e.g. OGT_HAEIN|P44687 Haemophilus influenzae (190 aa), FASTA scores: opt: 405, E(): 6.5e-20, (41.9% identity in 155 aa overlap). Contains PS00374 Methylated-DNA--protein-cysteine methyltransferase active site.
Functional categoryInformation pathways
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 whole cell lysates of M. tuberculosis H37Rv but not the culture filtrate or membrane protein fraction (See de Souza et al., 2011).
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). Two different M. tuberculosis H37Rv Rv1316c-Rv1317c deletion mutants (SID-H, and BS-SK which lacks an additional 246 bp of Rv1316c) have normal in vitro growth; both mutants are ~100-fold more sensitive to the cytotoxic effects of N-methyl-N'-nitro-N-nitroguanidine (MNNG); SID-H mutant shows ~100-fold higher mutation rate leading to rifampin resistance with MNNG treatment than wild-type; growth of mutants in mice (SID-H in C57BL/6, BS-SK in BALB/c) is comparable to wild-type (See Durbach et al., 2003).
Check for mutants available at TARGET website
Coordinates
TypeStartEndOrientation
CDS14771341477631-
Genomic sequence
Feature type Upstream flanking region (bp) Downstream flanking region (bp) Update
       
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv1316c|ogt
MIHYRTIDSPIGPLTLAGHGSVLTNLRMLEQTYEPSRTHWTPDPGAFSGAVDQLNAYFAGELTEFDVELDLRGTDFQQRVWKALLTIPYGETRSYGEIADQIGAPGAARAVGLANGHNPIAIIVPCHRVIGASGKLTGYGGGINRKRALLELEKSRAPADLTLFD