Abstract
We show that the disruption of one of the mycocerosic acid synthase (mas)-like genes, msl5 (pks8 plus pks17) in Mycobacterium tuberculosis H37Rv generates a mutant incapable of producing monomethyl branched unsaturated C(16) to C(20) fatty acids that are minor constituents of acyltrehaloses and sulfolipids. The msl5 mutation did not cause any significant change in the acyl lipid composition and also did not affect growth in culture, in mouse alveolar macrophage cell line MH-S, or in the murine lung.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Acyl Coenzyme A / metabolism*
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Acyltransferases / genetics
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Acyltransferases / metabolism*
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Animals
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Bacterial Proteins / genetics
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Bacterial Proteins / metabolism
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Cell Line
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Fatty Acids, Unsaturated / biosynthesis*
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Fatty Acids, Unsaturated / chemistry
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Lung / microbiology
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Macrophages, Alveolar / microbiology
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Mice
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Mice, Inbred C57BL
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Mutation
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Mycobacterium tuberculosis / genetics
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Mycobacterium tuberculosis / metabolism
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Mycobacterium tuberculosis / pathogenicity*
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Tuberculosis, Pulmonary / microbiology*
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Virulence
Substances
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Acyl Coenzyme A
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Bacterial Proteins
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Fatty Acids, Unsaturated
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methylmalonyl-coenzyme A
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Acyltransferases
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mycocerosic acid synthase