Unsaturated fatty acid biosynthesis and regulation.

Unsaturated fatty acid biosynthesis begins with the isomerization of trans-2-decenoyl-ACP to cis-3-decenoyl-ACP by FabA. Instead of being reduced, this intermediate is condensed with malonyl-ACP by FabB. The resulting unsaturated β-ketoacyl-ACP is processed analogous to its saturated counterpart until unsaturated C16 and C18 acyl-ACPs are made and incorporated into phospholipids. Unsaturated fatty acid biosynthesis is feedback-inhibited at the transcriptional level by FabR, which exhibits increased repression of transcription of fabA and fabB when bound to enoyl-ACP species [16], [17]. Expression of a thioesterase cleaves acyl-ACPs to generate FFA. BTE expression preferentially cleaves saturated C12-acyl-ACPs (solid blue arrow) and minorly cleaves unsaturated C12- (dashed blue arrow) and saturated and unsaturated C14-acyl-ACPs, thereby depleting saturated, long chain acyl-ACPs, the key regulatory signal for controlling fatty acid biosynthesis. As a result, flux through the saturated (prior to C10) and unsaturated pathway increases. Inset: the four arrows represent the elongation (FabB/FabF) (dashed arrow) in which the acyl chain represented by R grows by 2 carbons, ketoreduction (FabG), dehydration (FabZ), and enoyl reduction (FabI) reactions that comprise one round of fatty acid elongation and reduction.