TGS1 and infection: Deletion of tgs1, overexpression of citA and 14C-acetate tracer experiment indicated that triglyceride synthesis directed carbon sources away from the tricarboxylic acid cycle and other growth-promoting pathways, leading to decreases in bacterial growth and antibiotic efficacy, and that disruption of the metabolic switch disabled the growth arrest responding to stress, and resensitized bacteria to antibiotic treatment during infection [10].