Catalyzes the conversion of phosphatidic acid (PA) to CDP-diacylglycerol (CDP-DAG), an important precursor for the synthesis of phosphatidylinositol (PtdIns) and phosphatidylglycerol (PG) (PubMed:7816135, PubMed:24603715). Required for the regeneration of the signaling molecule phosphatidylinositol 4,5-bisphosphate (PtdInsP2) from PA and maintenance of its steady supply during signaling thus playing an essential role during phospholipase C-mediated transduction (PubMed:7816135). In the salivary glands and possibly other adipose tissues, function is essential for regulating cell growth and neutral lipid storage by coordinating PtdIns metabolism and insulin pathway activity (PubMed:24603715). Acts by positively regulating activity of the insulin pathway through synthesis of PtdIns, and in turn the insulin pathway up-regulates the synthesis of CdsA (PubMed:24603715). This CdsA-insulin positive feedback loop may be one of the mechanisms for coordinating cell growth and fat storage; switching to fat storage when cells reach homeostasis or converting from growth to fat storage under nutrient-poor conditions (PubMed:24603715). Required for spermatid individualization by regulating lipid compositions and lipid-mediated signaling during spermatogenesis (PubMed:26791243). a 1,2-diacyl-sn-glycero-3-phosphate + CTP + H(+) = a CDP-1,2-diacyl-sn-glycerol + diphosphate Phospholipid metabolism; CDP-diacylglycerol biosynthesis; CDP-diacylglycerol from sn-glycerol 3-phosphate: step 3/3. Retina. Localized to the photoreceptor neurons, both in the compound eyes and ocelli. In 3rd instar larvae, expressed in various tissues including the brain, salivary glands, fat body, proventriculus, hind gut, muscle, Malpighian tubules and tracheal tubes. Relatively low levels of expression in the brain compared to expression levels in the salivary gland, fat body and gut. Lethal during the late embryonic to early larval stages (PubMed:24603715). Hypomorphic mutants are viable but male adults are sterile, whereas female adults remain fertile (PubMed:26791243). Impairs spermatid individualization showing abnormal mitochondria morphology and defects in lipid compositions and lipid-mediated signaling (PubMed:26791243). RNAi-mediated knockdown results in low insulin pathway activity and defective cell growth in certain tissues (PubMed:24603715). Various non-adipose tissues display excessive fat accumulation such as the salivary glands, proventriculus, hind gut, Malpighian tubules and trachea (PubMed:24603715). In addition gross reduction in cell size results in smaller salivary glands, imaginal disks and brains compared to controls (PubMed:24603715). RNAi-mediated knockdown in both the salivary glands and fat body, results in decreased levels of phosphatidylinositol (PtdIns) in the whole larvae and in the salivary glands (PubMed:24603715). Whole larvae also display decreased levels of phosphatidylglycerol (PG) and increased levels of phosphatidic acid (PA) (PubMed:24603715). Larvae display low insulin pathway activity with reduced levels of phosphatidylinositol 4,5-bisphosphate (PtdInsP2) and phosphatidylinositol 3,4,5-trisphosphate (Ptdinsp3), and decreased levels of 'S-505' phosphorylated Akt1 (PubMed:24603715). RNAi-mediated knockdown specifically in the fat body, results in a decrease in PtdIns levels but there is no effect on the growth and neutral lipid storage in the fat body (PubMed:24603715). This is likely due to unknown compensatory mechanisms as there is an increase in the levels of diphosphate diacylglycerol and phosphatidylethanolamine in the fat body (PubMed:24603715). Belongs to the CDS family.