Host cholesterol modulates the generation and enrichment of persister population during Mycobacterium tuberculosis infection.

Post-translational modifications (PTMs) confer diversity to regulatory mechanisms that control various cellular pathways. Two of the most extensively studied PTMs are phosphorylation and acetylation. Together, they are known to regulate the stability and activity of proteins in both eukaryotes and prokaryotes. Lysine acetylation is known to regulate various cellular pathways conserved across species including mycobacteria. In order to confirm the cholesterol mediated deacetylation of anti-toxin in Mycobacteria, we did mass spectrometry of BCG strain overexpressing the toxin (vapC12)–antitoxin (vapB12)-His(6X) locus grown in glycerol and cholesterol media.