Acyltransferase required to remodel newly synthesized phospholipid cardiolipin (1',3'-bis-[1,2-diacyl-sn-glycero-3-phospho]-glycerol or CL), a key component of the mitochondrial inner membrane, with tissue specific acyl chains necessary for adequate mitochondrial function (PubMed:19114128, PubMed:21091282, PubMed:21068380, PubMed:23130124, PubMed:26114544, PubMed:30055293, PubMed:30389594). Its role in cellular physiology is to improve mitochondrial performance (By similarity). CL is critical for the coassembly of lipids and proteins in mitochondrial membranes, for instance, remodeling of the acyl groups of CL in the mitochondrial inner membrane affects the assembly and stability of respiratory chain complex IV and its supercomplex forms (By similarity). Catalyzes the transacylacion between phospholipids and lysophospholipids, with the highest rate being between phosphatidylcholine (1,2-diacyl-sn-glycero-3-phosphocholine or PC) and CL. Catalyzes both 1-acyl-sn-glycero-3-phosphocholine (lysophosphatidylcholine or LPC) reacylation and PC-CL transacylation, that means, it exchanges acyl groups between CL and PC by a combination of forward and reverse transacylations. Also catalyzes transacylations between other phospholipids such as phosphatidylethanolamine (1,2-diacyl-sn-glycero-3-phosphoethanolamine or PE) and CL, between PC and PE, and between PC and phosphatidate (1,2-diacyl-sn-glycero-3-phosphate or PA), although at lower rate. Not regiospecific, it transfers acyl groups into any of the sn-1 and sn-2 positions of the monolysocardiolipin (MLCL), which is an important prerequisite for uniformity and symmetry in CL acyl distribution. Cannot transacylate dilysocardiolipin (DLCL), thus, the role of MLCL is limited to that of an acyl acceptor. CoA-independent, it can reshuffle molecular species within a single phospholipid class. Redistributes fatty acids between MLCL, CL, and other lipids, which prolongs the half-life of CL. Its action is completely reversible, which allows for cyclic changes, such as fission and fusion or bending and flattening of the membrane. Hence, by contributing to the flexibility of the lipid composition, it plays an important role in the dynamics of mitochondria membranes. Essential for the final stage of spermatogenesis, spermatid individualization (By similarity). Required for the initiation of mitophagy (PubMed:25919711). Required to ensure progression of spermatocytes through meiosis (PubMed:26114544). 1,2-diacyl-sn-glycero-3-phospho-(1'-sn-glycerol) + a 1-acyl-sn-glycero-3-phosphate = 1-acyl-sn-glycero-3-phospho-(1'-sn-glycerol) + a 1,2-diacyl-sn-glycero-3-phosphate 1-(9Z-octadecenoyl)-sn-glycero-3-phosphate + 1-hexadecanoyl-2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phospho-(1'-sn-glycerol) = 1-(9Z)-octadecenoyl-2-(9Z,12Z)-octadecadienoyl-sn-glycero-3-phosphate + 1-hexadecanoyl-sn-glycero-3-phospho-(1'-sn-glycerol) 1'-[1,2-diacyl-sn-glycero-3-phospho],3'-[1-acyl-sn-glycero-3-phospho]-glycerol + a 1,2-diacyl-sn-glycero-3-phosphocholine = a 1-acyl-sn-glycero-3-phosphocholine + a cardiolipin 1-hexadecanoyl-2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphocholine + 1-hexadecanoyl-sn-glycero-3-phosphocholine = 1,2-dihexadecanoyl-sn-glycero-3-phosphocholine + 2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphocholine 1,2-di-(9Z-octadecenoyl)-sn-glycero-3-phosphocholine + 1-hexadecanoyl-sn-glycero-3-phosphocholine = 1-(9Z-octadecenoyl)-sn-glycero-3-phosphocholine + 1-hexadecanoyl-2-(9Z-octadecenoyl)-sn-glycero-3-phosphocholine Phospholipid metabolism. Associates with multiple protein complexes. Widely expressed with highest expression in skeletal muscle and kidney. The HXXXXD motif is essential for acyltransferase activity. Impaired cardiolipin (CL) metabolism with accumulation of monolysocardiolipin (MLCL) and reduction of mature CL in embryonic stem cells, male sterility, reduced testis size and disruption in progression of spermatocytes through meiosis (PubMed:26114544). Spermatocytes fail to progress past the pachytene stage of meiosis and have higher levels of DNA double strand damage and increased levels of endogenous retrotransposon activity (PubMed:26114544). RNAi-mediated knockdown results in prenatal and perinatal lethality, impaired CL metabolism resulting in absence of tetralineoyl-cardiolipin and accumulation of MLCL in cardiac and skeletal muscle, abnormal ultrastructure of mitochondria and mitochondrial-associated membranes, impaired skeletal muscle contractile properties, early diastolic dysfunction, and cardiac abnormalities such as myocardial thinning, hypertrabeculation, non-compaction, defective ventricular septation and left ventricular dilation (PubMed:21091282, PubMed:21068380, PubMed:23130124, PubMed:30389594). RNAi-mediated knockdown also results in impaired CL metabolism in the brain with reduced total CL levels and significantly increased MLCL levels, impaired brain mitochondrial respiration, elevated brain production of reactive oxygen species, significant memory deficiency, derangement of the hippocampal CA1 neuronal layer and elevated microglia activity (PubMed:30055293). Hepatic CL levels remain normal (PubMed:30055293). RNAi-mediated knockdown does not affect resting metabolic rate but markedly impairs oxygen consumption rates during exercise and diminishes mitochondrial complex III activity (PubMed:23616771). The enzyme was named after a masochistic character Tafazzi, once popular on Italian television, apparently due to the difficulty encountered for its identification and characterization. Belongs to the taffazin family.