FIG 5.

Model for BriC regulation of the FASII branch point in unsaturated fatty acid synthesis. The expression of briC is supported by either ComE, the RUPB1 enhancer, or cotranscription with the FabT regulon. Signaling through BriC results in the upregulation of fabT expression (this may be direct or indirect and is denoted with a dashed arrow). FabT is a transcriptional repressor of fabK, but not fabM, altering the branch point in FASII where FabK and FabM compete for the trans-2-decenoyl(C₁₀)-ACP intermediate (4). NADH-dependent FabK reduction produces a saturated acyl-ACP, whereas FabM isomerization creates an unsaturated acyl-ACP. Both intermediates are elongated by FabF to become saturated (SFA) and unsaturated (UFA) fatty acids, respectively. Tilting the competitive balance between FabK and FabM alters the UFA:SFA ratio.