A group led by a UF Health researcher gained a better understanding of the genetic activities that prevent muscle cells from repairing themselves. The findings apply to a rare congenital disorder known as early onset myopathy, areflexia, respiratory distress and dysphagia, or EMARDD, and have implications for other muscle disorders, including muscular dystrophy. The researchers identified a gene and mutation that function as a “switch” that prevents muscle cell proliferation in EMARDD patients. Using mouse muscle cells and mouse models, the researchers found a deficiency of a certain gene, known as Megf10, and the overabundance of a mutant form of this gene leads to reduced muscle cell growth and migration.