|A mouse model of FECD established via partial replacement of the mouse Tcf4 gene with the pathogenic human homologue, including non-coding DNA content.|
The first mouse model for FECD
Roughly 5% of the caucasion population will suffer vision loss as a result of Fuchs’ endothelial corneal dystrophy (FECD). Of these individuals, roughly 80% carry a mutation in the gene for Transcription Factor 4 (TCF4). This mutation (a CTG-repeat expansion) falls outside of the coding region of the gene, and is not fully understood. Generating the first mouse model of FECD, the Koob Laboratory at the University of Minnesota developed a set of mouse lines in which 134 kb of the mouse Tcf4 gene is replaced by the homologous 191 kb of human TCF4 either without (wild-type control) or with (experimental) the CTG expansion mutation. The replacement of such a large portion of DNA was accomplished using a proprietary technique developed in the lab. While most animal models generated are simplified and contain mostly coding portions of genes, this model includes the predominant (~99.5%) non-coding portions of TCF4. This FECD mouse model will facilitate research on the molecular contribution of disease mutations within their genomic context and better elucidate potential therapeutic interventions.
Phase of DevelopmentMouse lines to model FECD linked to TCF4 mutation and WT control have been established. Phenotype assessment and validation still in progress.
Ready for Licensing
This technology is now available for license! The University is excited to partner with industry to see this innovation reach its potential. Please contact Kenneth Karanja to share your business’ needs and your licensing interests in this technology.