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IN PRODUCTION

Cox7c, ortholog of human COX7C, encodes one of the smallest nuclear encoded subunits of cytochrome c oxidase, a single transmembrane helix added with subunits 6C and 8A during the final assembly module that seals the peripheral shell around the mitochondrially encoded catalytic core. Despite its size, this subunit is required for stable holoenzyme accumulation, so loss produces isolated complex IV deficiency with reduced cytochrome c oxidase activity and accumulated subassemblies, and de novo human variants have been reported in mitochondrial disease with encephalopathy. The design fork separates absolute requirement, tested by a floxed conditional null, from interface specific questions, tested by transmembrane substitutions that keep the subunit in place and better mimic patient alleles. No isoform paralog covers 7C in somatic tissues. Direct deletion with Nes-Cre, Ckmm-Cre, or inducible Rosa26-CreER, then combine COX histochemistry, spectrophotometric complex IV activity, respirometry, and blue native assembly analysis.

Cox7c conditional knockout mice carry a floxed allele so you delete function only where Cre is active. The germline allele stays intact until you cross to a tissue specific Cre. Labs reach for this design when a global knockout is lethal, when they need adult onset loss, or when regional redundancy hides a whole body phenotype.