Lef1, or lymphoid enhancer binding factor 1, is a nuclear mediator in the Wnt/β -catenin pathway, which is crucial for signal transduction from ectoderm to mesenchyme during the development of ectoderm-derived structures. It activates target gene expression in this pathway and is thus of great biological importance in various developmental and cellular processes [1].

Targeted inactivation of the Lef1 gene in mice results in a complete block of development of multiple ectodermal appendages, indicating its essential role in ectodermal development [1]. In a cartilage-specific Lef1 knockout (KO) mouse model for posttraumatic osteoarthritis (PTOA), Lef1 ablation alleviated cartilage mineralization, reduced OA severity and local pain, suggesting Lef1's role in cartilage mineralization and OA-related phenotypes [2].

In conclusion, Lef1 is vital for ectodermal development and plays a role in cartilage mineralization and OA. The Lef1 KO mouse models have been instrumental in revealing its functions in these disease-related biological processes, providing insights into potential therapeutic strategies for ectodermal dysplasia and OA.