Go to browser
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
FunctionInvolved in the adaptive response to alkylation damage in DNA caused by alkylating agents. Repairs the SP diastereomer of DNA methylphosphotriester lesions by a direct and irreversible transfer of the methyl group to one of its own cysteine residues. The methylated ALKA protein acts as a positive regulator of its own synthesis, as well as that of other proteins.
ProductProbable bifunctional regulatory protein and DNA repair enzyme AlkA (regulatory protein of adaptative response) (methylphosphotriester-DNA--protein-cysteine S-methyltransferase)
CommentsRv1317c, (MTCY130.02c), len: 496 aa. Probable alkA (alternate gene name: ada), bifunctional regulatory protein (see citation below) and DNA repair enzyme, similar to 3MG2_ECOLI|P04395 dna-3-methyladenine glycosidase II from Escherichia coli (282 aa), FASTA scores, opt: 437, E(): 8.6e-22, (32.8% identity in 293 aa overlap), also similar to other ada proteins e.g. ADA_SALTY|P26189 Salmonella typhimurium (352 aa), FASTA scores: E(): 5.3e-08, (35.9% identity in 156 aa overlap). Contains PS00041 Bacterial regulatory proteins, araC family signature.
Functional categoryInformation pathways
ProteomicsIdentified in the cell wall and cell membrane fractions of M. tuberculosis H37Rv using 2DLC/MS (See Mawuenyega et al., 2005). 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). Non-essential gene for in vitro growth of H37Rv, by Himar1 transposon mutagenesis (See Griffin et al., 2011). 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
CDS14776281479118-
Genomic sequence
Feature type Upstream flanking region (bp) Downstream flanking region (bp) Update
       
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv1317c|alkA
VHDDFERCYRAIQSKDARFDGWFVVAVLTTGVYCRPSCPVRPPFARNVRFLPTAAAAQGEGFRACKRCRPDASPGSPEWNVRSDVVARAMRLIADGTVDRDGVSGLAAQLGYTIRQLERLLQAVVGAGPLALARAQRMQTARVLIETTNLPFGDVAFAAGFSSIRQFNDTVRLACDGTPTALRARAAARFESATASAGTVSLRLPVRAPFAFEGVFGHLAATAVPGCEEVRDGAYRRTLRLPWGNGIVSLTPAPDHVRCLLVLDDFRDLMTATARCRRLLDLDADPEAIVEALGADPDLRAVVGKAPGQRIPRTVDEAEFAVRAVLAQQVSTKAASTHAGRLVAAYGRPVHDRHGALTHTFPSIEQLAEIDPGHLAVPKARQRTINALVASLADKSLVLDAGCDWQRARGQLLALPGVGPWTAEVIAMRGLGDPDAFPASDLGLRLAAKKLGLPAQRRALTVHSARWRPWRSYATQHLWTTLEHPVNQWPPQEKIA