The human congenital malformation cleft lip with or without cleft palate (CL/P) seems to be genetically distinct from isolated cleft palate. However, recent data indicate that the bone morphogenetic protein (Bmp) signalling pathway may be involved in both forms of orofacial clefting. Liu and co-workers now report that Bmp signalling has distinct functions in lip and palate fusion in mice (see p. 1453). The researchers show that conditional inactivation of the type 1 Bmp receptor Bmpr1a in the facial primordia produces mice with bilateral CL/P. Diminished cell proliferation in the maxillary process mesenchyme underlies the palate defects, but increased apoptosis in the medial nasal process is responsible for the cleft lip. Furthermore, conditional inactivation of Bmp4 produces isolated cleft lip, indicating that a Bmp4-Bmpr1a genetic pathway functions in lip fusion. These results will aid in unravelling the mechanisms underlying human clefting conditions.
- © 2005.