FGFR3-GOF mice conditionally express a mouse Fgfr3 (fibroblast growth factor receptor 3) altered to become constitutively active and an EGFP from the broadly-expressed CAG promoter upon cre-mediated excision of a loxP-flanked Stop cassette. Fgfr3 belongs to a family of FGF receptors, and, in particular, Fgfr3 binds to acidic and basic fibroblast growth hormone. Mutations in this gene are associated with craniosynostosis and multiple types of skeletal dysplasia. Mice hemizygous for the transgene are viable and fertile. When the floxed Stop is removed using an astrocyte specific cre transgene, moderate over-expression of the K650E mutant activates FGF signaling in adult astrocytes following traumatic cortical injury to the neocortex. FGFR3-GOF mice exhibit less GFAP straining (to visualize reactive astrocytes) 3 days after injury (peak activation) as compared to controls. Twenty days after injury FGFR3-GOF mice have developed fewer reactive astrocytes and have thinner and less compact scars without affecting neuron survival. In addition, although astrocyte activation is suppressed, proliferation of astrocytes around the injury site is increased. This mutant mouse strain may be useful in studies related to astrocyte activation and other systems involving fibroblast growth factor signaling.

FGFR3-GOF mice conditionally express a mouse Fgfr3 (fibroblast growth factor receptor 3) altered to become constitutively active and an EGFP from the CAG promoter. This mutant mouse strain may be useful in studies related to astrocyte activation and other systems involving fibroblast growth factor signaling.

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