Myodegeneration in EDA-A2 Transgenic Mice Is Prevented by XEDAR Deficiency

The study investigated the roles of EDA-A1 and EDA-A2, members of the tumor necrosis factor family, in mice. EDA-A1, which binds to EDAR, was known to be crucial for the development of sweat glands, hair, and teeth, with mutations causing hypohidrotic ectodermal dysplasia. The role of EDA-A2, which binds to XEDAR, was less understood. Researchers created XEDAR-deficient mice and transgenic mice expressing EDA-A1 or EDA-A2. They found that XEDAR-deficient mice were similar to wild-type mice, but EDA-A2 transgenic mice showed multifocal myodegeneration, a condition not present without XEDAR. EDA-A1 transgenic mice had unaffected skeletal muscle but showed changes in sebaceous glands, supporting EDA-A1's role in their development. The findings suggested that while XEDAR signals were not essential for ectoderm-derived organ development, they might be involved in skeletal muscle maintenance.