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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
FunctionInvolved in cholesterol metabolism [catalytic activity: cholesterol + O(2) = cholest-4-en-3-one + H(2)O(2)].
ProductCholesterol oxidase ChoD (cholesterol-O2 oxidoreductase)
CommentsRv3409c, (MTCY78.19), len: 578 aa. ChoD, cholesterol oxidase, equivalent to Q9CCV1|CHOD|ML0389 (alias Q59530|CHOD|B1620_C3_240) putative cholesterol oxidase from Mycobacterium leprae (569 aa), FASTA scores: opt: 3510, E(): 3.8e-198, (88.6% identity in 569 aa overlap). Belongs to the GMC oxidoreductases family. Cofactor: FAD flavoprotein. Contains PS00017 ATP/GTP-binding site motif A.
Functional categoryLipid metabolism
ProteomicsIdentified in the membrane fraction of M. tuberculosis H37Rv using nanoLC-MS/MS (See Xiong et al., 2005). Identified by mass spectrometry in Triton X-114 extracts of M. tuberculosis H37Rv (See Malen et al., 2010). Identified by mass spectrometry in the membrane protein fraction of M. tuberculosis H37Rv but not the culture filtrate or membrane protein fraction (See de Souza et al., 2011).
TranscriptomicsmRNA identified by microarray analysis; transcription repressed at low pH in vitro conditions, which may mimic an environmental signal encountered by phagocytosed bacteria (see citation below).
MutantNon-essential gene for in vitro growth of H37Rv in a MtbYM rich medium, by Himar1 transposon mutagenesis (see Minato et al. 2019). Disruption of this gene provides a growth advantage 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). Non-essential gene for in vitro growth of H37Rv, by Himar1 transposon mutagenesis (See Griffin et al., 2011). Deletion of choD in M. tuberculosis results in attenuation in vitro in mouse peritoneal macrophages, and in vivo in C57BL/6 mouse lungs and spleens (see Brzostek et al., 2007).
Check for mutants available at TARGET website
Coordinates
TypeStartEndOrientation
CDS38269913828727-
Genomic sequence
Feature type Upstream flanking region (bp) Downstream flanking region (bp) Update
       
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv3409c|choD
MKPDYDVLIIGSGFGGSVTALRLTEKGYRVGVLEAGRRFSDEEFAKTSWDLRKFLWAPRLGCYGIQRIHPLRNVMILAGAGVGGGSLNYANTLYVPPEPFFADQQWSHITDWRGELMPHYQQAQRMLGVVQNPTFTDADRIVKEVADEMGFGDTWVPTPVGVFFGPDGTKTPGKTVPDPYFGGAGPARTGCLECGCCMTGCRHGAKNTLVKNYLGLAESAGAQVIPMTTVKGFERRSDGLWEVRTVRTGSWLRRDRRTFTATQLVLAAGTWGTQHLLFKMRDRGRLPGLSKRLGVLTRTNSESIVGAATLKVNPDLDLTHGVAITSSIHPTADTHIEPVRYGKGSNAMGLLQTLMTDGSGPQGTDVPRWRQLLQTASQDPRGTIRMLNPRQWSERTVIALVMQHLDNSITTFTKRGKLGIRWYSSKQGHGEPNPTWIPIGNQVTRRIAAKIDGVAGGTWGELFNIPLTAHFLGGAVIGDDPEHGVIDPYHRVYGYPTLYVVDGAAISANLGVNPSLSIAAQAERAASLWPNKGETDRRPPQGEPYRRLAPIQPAHPVVPADAPGALRWLPIDPVSNAG
      
Bibliography