Catalyzes the biosynthesis of phosphatidylinositol (PtdIns) as well as PtdIns:inositol exchange reaction (PubMed:17151285, PubMed:24828534, PubMed:24603715). May thus act to reduce an excessive cellular PtdIns content (By similarity). The exchange activity is due to the reverse reaction of PtdIns synthase and is dependent on CMP, which is tightly bound to the enzyme (By similarity). Required for the regeneration of the signaling molecule phosphatidylinositol 4,5-bisphosphate (PtdInsP2) from phosphatidic acid (PA) and maintenance of its steady supply during signaling, thus playing an essential role during phospholipase C-mediated transduction (PubMed:17151285). This function is essential in photoreceptors for light-activated recycling of PtdInsP2 during phototransduction (PubMed:17151285). As a key enzyme of the phosphoinositide pathway, indirectly involved in the polarized secretion of basal membrane (BM) proteins in follicle epithelial (FE) cells through promoting PtdInsP2 synthesis in the apical and lateral plasma membranes of FE cells (PubMed:24828534). PtdInsP2 controls the localization of Crag and perhaps the localization and expression of strat, both of which are essential for restricting the secretion of BM proteins to the basal surface (PubMed:24828534, PubMed:28228250). a CDP-1,2-diacyl-sn-glycerol + myo-inositol = a 1,2-diacyl-sn-glycero-3-phospho-(1D-myo-inositol) + CMP + H(+) Although Mn(2+) can act as a cofactor, it is much less effective than Mg(2+). In follicle cells, detected at the apical and lateral regions of the plasma membrane. In adults, expression is higher in the head than in the body (at protein level). Expressed throughout development, with low levels of expression in embryos and 1st instar larvae, and highest levels of expression in adults (at protein level). Embryonic lethal (PubMed:17151285). In follicle cells, abnormal apical accumulation of the basal membrane (BM) proteins trol and vkg (PubMed:24828534). Decreased expression of strat in follicle epithelial cells (PubMed:28228250). RNAi-mediated knockdown in both larval salivary glands and fat body, results in small salivary glands that accumulate lipid droplets. This is likely due to the observed decrease in PtdIns levels that would lead to low insulin pathway activity and defective cell growth. RNAi-mediated knockdown in the fat body also results in a decrease in PtdIns levels in the fat body and a decrease in fat body size (PubMed:24603715). Belongs to the CDP-alcohol phosphatidyltransferase class-I family.