Mitochondrial citramalyl-CoA lyase indirectly involved in the vitamin B12 metabolism (PubMed:29056341). Converts citramalyl-CoA into acetyl-CoA and pyruvate in the C5-dicarboxylate catabolism pathway (PubMed:29056341). The C5-dicarboxylate catabolism pathway is required to detoxify itaconate, a vitamin B12-poisoning metabolite (PubMed:29056341). Also acts as a malate synthase in vitro, converting glyoxylate and acetyl-CoA to malate (PubMed:29056341, PubMed:24334609). Also displays malyl-CoA thioesterase activity (PubMed:29056341). Also acts as a beta-methylmalate synthase in vitro, by mediating conversion of glyoxylate and propionyl-CoA to beta-methylmalate (PubMed:24334609, PubMed:29056341). Also has very weak citramalate synthase activity in vitro (PubMed:24334609, PubMed:29056341). acetyl-CoA + glyoxylate + H2O = (S)-malate + CoA + H(+) glyoxylate + H2O + propanoyl-CoA = 3-methylmalate + CoA + H(+) (3S)-citramalyl-CoA = acetyl-CoA + pyruvate (S)-malyl-CoA + H2O = (S)-malate + CoA + H(+) Binds 1 Mg(2+) ion per subunit. kcat is 0.12 sec(-1) for malate synthase reaction (PubMed:24334609). kcat is 0.09 sec(-1) for beta-methylmalate synthase reaction (PubMed:24334609). kcat is 0.135 sec(-1) for beta-methylmalate synthase reaction (PubMed:29056341). kcat is 0.146 sec(-1) for malate synthase reaction (PubMed:29056341). kcat is 0.08 sec(-1) for citramalate synthase reaction (PubMed:29056341). kcat is 14.1 sec(-1) for citramalyl-CoA lyase reaction (PubMed:29056341). Homotrimer. The protein is absent in 2.7% of the human population due to a loss-of-function polymorphism (rs41281112) that changes Arg-259 to a premature stop codon, leading to loss of the protein product (PubMed:23754956, PubMed:24334609). This polymorphism is associated with reduction of circulating vitamin B12 (PubMed:23754956, PubMed:24334609). The reduction of circulating vitamin B12 is caused by accumulation of citramalyl-CoA, an intermediate in the C5-dicarboxylate metabolic pathway that includes itaconate (PubMed:29056341). Itaconate acting as a vitamin B12-poisoning metabolite that inactivates the mitochondrial methylglutaconyl-CoA hydratase (AUH) enzyme (PubMed:29056341). Belongs to the HpcH/HpaI aldolase family. Citrate lyase beta subunit-like subfamily. This organism lacks the other subunits that are necessary for ATP-independent citrate lyase activity. Even though this protein has clear similarity to citrate lyase beta subunit, it is expected to have a somewhat different enzyme activity.