Exogenous fatty acids inhibit fatty acid synthesis by competing with endogenously generated substrates for phospholipid synthesis in Escherichia coli.

Exogenous fatty acids are directly incorporated into bacterial membranes, heavily influencing cell envelope properties, antibiotic susceptibility, and bacterial ecology. Here, we quantify fatty acid biosynthesis metabolites and enzymes of the fatty acid synthesis pathway to determine how exogenous fatty acids inhibit fatty acid synthesis in Escherichia coli. We find that acyl-CoA synthesized from exogenous fatty acids rapidly increases concentrations of long-chain acyl-acyl carrier protein (acyl-ACP), which inhibits fatty acid synthesis initiation.

A temperature-sensitive metabolic valve and a transcriptional feedback loop drive rapid homeoviscous adaptation in Escherichia coli.

All free-living microorganisms homeostatically maintain the fluidity of their membranes by adapting lipid composition to environmental temperatures. Here, we quantify enzymes and metabolic intermediates of the Escherichia coli fatty acid and phospholipid synthesis pathways, to describe how this organism measures temperature and restores optimal membrane fluidity within a single generation after a temperature shock. A first element of this regulatory system is a temperature-sensitive metabolic valve that allocates flux between the saturated and unsaturated fatty acid synthesis pathways via the branchpoint enzymes FabI and FabB.