Kctd15 Conditional Knockout mouse models

Kctd15, the mouse ortholog of human KCTD15, encodes a BTB and POZ domain protein that oligomerizes into pentamers and acts both as a Cullin3 E3 ligase adaptor and as a direct inhibitor of AP-2 transcription factors, a mechanism first defined in neural crest induction where KCTD15 restricts the crest domain at the neural plate border. In vertebrate development it also modulates Wnt and Nodal signaling, and in the hypothalamus it has been implicated in the melanocortin pathway, consistent with human GWAS signals near KCTD15 for body mass index and obesity risk. Related family members KCTD1 and KCTD15 share the AP-2 inhibitory activity, and the closely related KCTD12 and KCTD17 diverge functionally, so paralog-aware design matters. Conditional nulls with Wnt1-Cre address neural crest derivatives, while hypothalamic or Pomc-restricted deletion addresses energy balance, and Cullin3-binding-deficient knockins separate ligase-dependent from transcription factor-binding functions. Choose the allele that matches whether the endpoint is craniofacial patterning, adiposity, or transcriptional output.

Kctd15 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.