Phospholipid biosynthesis by Plasmodium knowlesi-infected erythrocytes: the incorporation of phospohlipid precursors and the identification of previously undetected metabolic pathways.

Metabolic pathways leading to phospholipid biosynthesis in Plasmodium-infected simian erythrocytes were tested and quantified by incubating leucocyte-free erythrocytes in the presence of labelled precursors. Plasma fatty acids and lysophospholipids both served as sources of the fatty acids required for cellular phospholipid biosynthesis. However, the entry of free fatty acids and lysophospholipids appeared to be controlled by a competitive mechanism. A powerful deacylase-acylase system was detected, the nature and specificity of which remain to be defined. Glycerol-3-phosphate incorporation into cellular lipids accounted for most of the new phospholipid molecules formed in parasitized cells, and into cellular lipids accounted for most of the new phospholipid molecules formed in parasitized cells, and this compound, rather than the lysophospholipids, appeared to be the natural acceptor of the acyl groups. By incorporation of nitrogenous bases into cellular phospholipids, we identified significant pathways not previously detected in Plasmodium-infected erythrocytes: the formation of phosphatidylethanolamine by phosphatidylserine decarboxylation, and the formation of phosphatidylcholine by the methylation of phosphatidylethanolamine. These results, associated with the absence of lipid synthesis in host cells, mean that the enzymes controlling these two pathways could serve as enzymatic markers of parasites.