Fzd2 Conditional Knockout mouse models

Fzd2, mouse ortholog of human FZD2, encodes a class F seven transmembrane receptor closely related to FZD1 and FZD7, binding Wnt ligands through its cysteine rich domain and coupling to both canonical beta-catenin signaling via LRP5 and LRP6 and to planar cell polarity signaling through Dishevelled, DAAM1 and RHOA with ROCK and JNK output. Heterozygous truncating variants near the C-terminal KTXXXW and PDZ binding region cause autosomal dominant Robinow syndrome and omodysplasia, and these act as dominant alleles rather than simple loss of function, which means a conventional null will not reproduce the human disease and a targeted truncation knockin is required. FZD2 is also induced during epithelial to mesenchymal transition and supports STAT3 dependent invasion in carcinoma. Single nulls are viable with cleft palate at low penetrance, but combined Fzd1 and Fzd2 deletion produces highly penetrant palatal clefting, confirming real redundancy. Match design to question, using truncation knockins for skeletal dysplasia and compound conditional alleles for developmental requirement.

Conditional deletion of Fzd2 limits the genetic change to the lineage you choose. That helps in oncology, immunology, and metabolic work where systemic loss would muddy the read. After you confirm Cre specificity, crossing to Fzd2 floxed stock yields usable cohorts.