Fgf16 Conditional Knockout mouse models

Fgf16, ortholog of human FGF16, encodes a secreted FGF9 subfamily ligand that, unlike most paracrine members, dimerizes in a way that limits heparan sulfate binding and diffusion, and it signals preferentially through FGFR1c, FGFR2c, FGFR3c, and FGFR4 with FRS2 to ERK output. Expression concentrates in embryonic and adult cardiomyocytes and brown adipose tissue, where it supports cardiomyocyte proliferation during ventricular growth and modulates hypertrophic and injury responses, and additional signal in developing limb correlates with human phenotypes. Hemizygous human loss-of-function variants cause X-linked metacarpal 4 and 5 fusion, and the mouse locus is likewise X-linked, so hemizygous male, homozygous female, and mosaic heterozygous female comparisons must be built into the design. Nulls are viable, making constitutive deletion tractable for cardiac stress testing, while conditional floxed alleles with Myh6-Cre or Adipoq-Cre attribute effects to muscle versus fat. Substantial overlap with Fgf9 and Fgf20 at shared c-isoform receptors argues for compound alleles when scoring proliferation endpoints.

Conditional deletion of Fgf16 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 Fgf16 floxed stock yields usable cohorts.