Involved in the gluconeogenesis, in growth on fatty acids and is important for initiation of infection in the macrophages. Catalyzes the GTP-dependent conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP), the rate-limiting step in the metabolic pathway that produces glucose from lactate and other precursors derived from the citric acid cycle. GTP + oxaloacetate = CO2 + GDP + phosphoenolpyruvate Binds 1 Mn(2+) ion per subunit. Carbohydrate biosynthesis; gluconeogenesis. Monomer. Cells lacking this gene are unable to grow in the absence of an external carbon source when grown with fatty acids acetate, valerate, or butyrate as the sole carbon source. This mutant also fails to replicate in mouse lungs. PEPCK depletion during the chronic phase of infection results in mycobacterial clearance. The number of CD4 T-cells is increased in the PEPCK immunized mice although the change of the number of CD8 T-cells is not significant. The cytokines IFN-gamma (IFNG), IL-12 (IL12A or IL12B) and TNF-alpha (TNF) are increased significantly in the mice immunized with PEPCK relative to those immunized with incomplete adjuvant. Belongs to the phosphoenolpyruvate carboxykinase [GTP] family.