Cleft lip, with or without cleft palate, occurs in around 1 in 700 human newborns, but little is known about the mechanisms involved. Now, on p. 3161, Chengji Zhou and colleagues identify the Wnt co-receptor Lrp6 as being crucial for normal lip morphogenesis in mice. All mice in which Lrp6 is deleted develop a cleft lip with cleft palate. These defects correlate with blocked Wnt/β-catenin signalling and with reduced cell proliferation in the primordia of the lip and palate (known as the orofacial primordia) earlier in development. Concomitantly with reduced Wnt/β-catenin signalling, the expression of the homeobox genes Msx1 and Msx2, which are important for mesenchyme proliferation, is decreased in the orofacial primordia. Conversely,the expression of Raldh3, which encodes a retinoic acid-synthesising enzyme that counteracts tissue fusion, expands. The authors demonstrate that Msx1 and Msx2 are direct targets of Wnt/β-catenin signalling and conclude that Lrp6-mediated Wnt/β-catenin signalling regulates lip formation and fusion by balancing the activities of Msx1 and Msx2 with the opposing activity of Raldh3.
Lrp6 fuses lips
Lrp6 fuses lips. Development 15 September 2009; 136 (18): e1805. doi:
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