Fig. 5.

Model for the proposed roles of TgACSs in parasite host-adaptation and lipid metabolism. Fatty acids (FA) from the host, extracellular environment, and directly from the parasite are incorporated into the glycerolipid pathway of the parasite. They are esterified onto a glycerol-3-phosphate (G-3-P) by acyltransferase (ATS) like ATS1, ATS2, and AGPAT to form lysophosphatidic acid (LPA) with backbone and phosphatidic acid (PA), respectively. LIPIN is a phosphatase responsible for dephosphorylation of PA to diacylglycerol (DAG) onto which another FA is attached to form triacylglycerol (TAG) by DGAT. FA must be activated to allow for their utilization by ATSs, this is facilitated by acyl-CoA synthetases (ACSs). The downregulation of TgACS3 leads to effects in intracellular parasites in a high host nutrient environment. There is an “over scavenging” effect that leads to an increase in host-derived and global FFA levels, but this is coupled with a decrease in host-derived TAG, DAG, and phospholipid (PL) levels.