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Literature summary extracted from

  • Dubey, V.S.; Sirakova, T.D.; Kolattukudy, P.E.
    Disruption of msl3 abolishes the synthesis of mycolipanoic and mycolipenic acids required for polyacyltrehalose synthesis in Mycobacterium tuberculosis H37Rv and causes cell aggregation (2002), Mol. Microbiol., 45, 1451-1459.
    View publication on PubMed

Molecular Weight [Da]

EC Number Molecular Weight [Da] Molecular Weight Maximum [Da] Comment Organism
2.3.1.252 220300
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 calculated from sequence of pks3 and pks4. The genes originally designated pks3 and pks4 in Mycobacterium tuberculosis genome jointly constitute a single gene (msl3) encoding a 220000 Da protein Mycobacterium tuberculosis

Organism

EC Number Organism UniProt Comment Textmining
2.3.1.252 Mycobacterium tuberculosis A0A089QRB9
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2.3.1.252 Mycobacterium tuberculosis H37Rv A0A089QRB9
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Synonyms

EC Number Synonyms Comment Organism
2.3.1.252 Msl3 gene name. The genes originally designated pks3 and pks4 in Mycobacterium tuberculosis genome jointly constitute a single gene (msl3) encoding a 220000 Da protein Mycobacterium tuberculosis

General Information

EC Number General Information Comment Organism
2.3.1.252 malfunction Msl3 is disrupted using a phage mediated delivery system. Biochemical analysis shows that the msl3 mutant does not produce mycolipanoic acids and mycolipenic (phthienoic) acids, the major constituents of polyacyl trehaloses and thus lacks this cell wall lipid, but synthesizes all of the other classes of lipids. The absence of the major acyl chains that anchor the surface-exposed acyltrehaloses causes a novel growth morphology. The cells stick to each other, most probably via the intercellular interaction between the exposed hydrophobic cell surfaces, manifesting a bead-like growth morphology without affecting the overall growth rate Mycobacterium tuberculosis