Cyp26c1 Conditional Knockout mouse models

Cyp26c1, mouse ortholog of human CYP26C1, encodes the third retinoic acid hydroxylase of the family, distinguished by its ability to act on both all-trans and 9-cis retinoic acid and by a sharply restricted expression pattern in rhombomeres 2 and 4, first branchial arch, and inner ear, where it refines local retinoid clearance beyond what the other isoforms supply. Human variants combined with CYP26B1 lesions have been reported in focal facial dermal dysplasia, consistent with an additive retinoid-clearance requirement. Single nulls are viable and essentially normal, which is the central design fact: informative genetics requires compound deletion with Cyp26a1, where double mutants show markedly enhanced hindbrain and rostral patterning defects that neither allele produces alone. Accordingly, invest in a floxed allele that can be combined sequentially rather than a plain knockout, and consider enzyme-dead knockins when substrate preference between all-trans and 9-cis isomers is the question. Reserve humanization for inhibitor selectivity profiling against defined craniofacial or otic endpoints.

Cyp26c1 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.