Cyp26b1 Conditional Knockout mouse models

Encoding a second retinoic acid 4-hydroxylase, Cyp26b1 is the mouse ortholog of human CYP26B1 and shields specific tissues from retinoid exposure rather than shaping the trunk axis, most decisively in the fetal testis, where its expression in Sertoli and interstitial cells degrades retinoic acid to keep male germ cells from entering meiosis prematurely, and in skin, where it restrains epidermal retinoid tone. Germline deletion is lethal shortly after birth with a severe permeability barrier defect, limb and craniofacial abnormalities, and ectopic germ cell meiosis, while biallelic human variants cause craniosynostosis with radiohumeral fusion. That neonatal lethality makes conditional floxed alleles essential for adult skin, immune, and spermatogenic questions, and catalytically inactive knockins separate hydroxylase output from protein presence. Because Cyp26a1 and Cyp26c1 clear the same substrate in overlapping fields such as hindbrain, single-locus loss can be partially buffered. Match tissue-restricted Cre drivers, Krt14-Cre for barrier or Amh-Cre for Sertoli cells, to the specific retinoid threshold being tested.

A floxed Cyp26b1 allele paired with Cre gives spatial control that whole body knockouts cannot offer. People use it to separate developmental roles from adult homeostasis, to model somatic mutations, and to match disease that begins in one organ.