CTP-dependent diacylglycerol kinase that catalyzes the phosphorylation of diacylglycerol (DAG) to phosphatidate (PA). Controls phosphatidate levels at the nuclear envelope. Counteracts the activity of PA phosphatase PAH1/SMP2, controlling the levels of PA and DAG for the synthesis of triacylglycerol and membrane phospholipids (PubMed:18458075, PubMed:27834677). May be involved in vesicle trafficking between the endoplasmic reticulum and the Golgi apparatus (PubMed:11481671). Required to convert triacylglycerol-derived DAG to PA for phospholipid synthesis during growth resumption from stationary phase in the absence of de novo fatty acid synthesis (PubMed:21071438). Involved in the resistance to nickel chloride and nalidixic acid (PubMed:10407277). a 1,2-diacyl-sn-glycerol + CTP = a 1,2-diacyl-sn-glycero-3-phosphate + CDP + H(+) 1,2-di-(9Z-octadecenoyl)-sn-glycerol + CTP = 1,2-di-(9Z-octadecenoyl)-sn-glycero-3-phosphate + CDP + H(+) Inhibited by N-ethylmaleimide, dCTP, and sphingoid bases including sphinganine, sphingosine and phytosphingosine. DAG pyrophosphate, cardiolipin, CDP-DAG, and lyso-PA inhibited activity by 23-66%. Also inhibited by Ca(2+) concentrations of more than 1 mM, by addition of EDTA or EGTA at 5 mM, and by 5 mM Mn(2+) and Zn(2+). Stimulated by major membrane phospholipids including phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine, phosphatidylglycerol, and phosphatidate. Also stimulated to a maximum by addition of TritonX-100 at a concentration of 1 mM, followed by an apparent inhibition of activity at concentrations above 1 mM. Optimum pH is 7.0-7.5. Maximum activity at 30 degrees Celsius. Labile above 40 degrees Celsius. CKII-mediated phosphorylation of Ser-45 and Ser-46 regulates its function in the production of PA. Present with 784 molecules/cell in log phase SD medium. Rescues the lethality of dephosphorylated PAH1/SMP2. Overexpression causes the appearance of phosphatidate-enriched membranes around the nucleus, leading to expansion of the nuclear membrane without proliferation of the cortical endoplasmic reticulum membrane. Deletion restores normal nuclear structure in PAH1/SMP2 deleted cells and returns the level of INO1 mRNA to normal. Deletion does not affect the abnormal levels of phosphatidylinositol and major neutral lipid triacylglycerol seen in the PAH1/SMP2 deletion mutant. Belongs to the DGK1 family.