People with fibrodysplasia ossificans progressiva (FOP) grow bone where it doesn’t belong, such as across joints, in soft tissues, and on top of the normal skeleton. The disease is a consequence of inappropriate signaling between cells via the bone morphogenetic protein signaling pathway (also found in corals). In the January issue of the journal Developmental Dynamics, Kristi Wharton, associate professor of medical science, and graduate student Viet Le, reported using a fruit fly genetic model of the disease to find that the mutant form of the ALK2 type I receptor protein in FOP patients requires the presence of a second type II receptor to transmit its hyperactive signal that ultimately leads to unwanted bone growth. “This interaction between the type II receptor and the hyperactivated mutant type I receptor is required to generate inappropriate signaling,” Wharton said. “Its identification provides a new target for the development of therapeutic drugs for the treatment of FOP.”

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