Fgf10 Conditional Knockout mouse models

Fgf10, ortholog of human FGF10, encodes a mesenchymally expressed paracrine ligand with strong heparan sulfate affinity that signals with high selectivity through the FGFR2b splice variant on adjacent epithelium, driving FRS2 to ERK output and constituting the reciprocal mesenchymal arm of the FGF10 to FGFR2b to SHH loop that governs branching morphogenesis. It is required for lung bud initiation and outgrowth, limb bud induction, and development of salivary, lacrimal, mammary, and pancreatic epithelium, and it maintains adult alveolar and airway progenitors. Germline nulls die at birth with complete lung agenesis and absent limbs, so conditional floxed alleles are mandatory for postnatal regeneration studies. Human heterozygous loss causes lacrimo-auriculo-dento-digital syndrome and aplasia of lacrimal and salivary glands, making hypomorphic or heterozygous designs the closer disease match. The related ligand FGF7 shares FGFR2b and can partially substitute in glandular epithelium, so compound alleles clarify attribution. Pair the flox with Tbx4-rtTA or Dermo1-Cre depending on the tissue endpoint.

Fgf10 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.