作者: L. Song , Y. Li , K. Wang , Y.-Z. Wang , A. Molotkov
DOI: 10.1242/DEV.037440
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摘要: Neither the mechanisms that govern lip morphogenesis nor cause of cleft are well understood. We report genetic inactivation Lrp6, a co-receptor Wnt/β-catenin signaling pathway, leads to with palate. The activity Wnt reporter is blocked in orofacial primordia by Lrp6 deletion mice. morphological dynamic required for normal formation and fusion disrupted these mutants. expression homeobox genes Msx1 Msx2 dramatically reduced mutants, which prevents outgrowth primordia, especially site. further demonstrate (but not their potential regulator Bmp4 ) downstream targets pathway during fusion. By contrast, `fusion-resistant' gene, Raldh3 (also known as Aldh1a3 ), encodes retinoic acid-synthesizing enzyme ectopically expressed upper Lrp6-deficient embryos, indicating region-specific role repressing acid signaling. Thus, Lrp6-mediated development orchestrating two distinctively different morphogenetic movements.