FdmR was identified as a long-chain acyl-coenzyme A (acyl-CoA)–responsive repressor of genes involved in fatty acid degradation and modification. The mutant showed defective growth but high substrate consumption on fatty acids. marinum mutant deficient in FdmR was severely attenuated in zebrafish larvae and adult zebrafish. Here, we identified a TetR-family transcriptional factor, FdmR, as the key regulator of fatty acid catabolism in the pathogen Mycobacterium marinum by combining use of transcriptomics, chromatin immunoprecipitation followed by sequencing, dynamic 13C-based flux analysis, metabolomics, and lipidomics. How mycobacterial cells regulate the catabolism of fatty acids to serve the pathogenicity, however, remains unknown. Host-derived fatty acids are an important carbon source for pathogenic mycobacteria during infection.
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