Abstract
Mammalian palate development is regulated by complex processes. Many cellular and molecular events, such as cell proliferation, apoptosis, cell migration and the epithelial mesenchymal transition, regulate proper palate development and some abnormalities in palate development lead to cleft palate. Various developmental disorders, such as cleft palate and disorders of the lung, kidney and heart, are known to be associated with ciliary defects. Pitchfork, a mouse embryonic node gene, is associated with ciliary targeting complexes located at the basal body during primary cilia disassembly. To determine the function of Pitchfork during palate development, we examine Pitchfork expression patterns and morphological changes in the developing secondary palate after Pitchfork over-expression. From embryonic day 12.5 (E12.5) to E13.5 in mice, Pitchfork was highly expressed in the developing mouse secondary palate. Morphological differences were observed in vitro in cultured palates in the Pitchfork over-expression group compared with the control group. Pitchfork over-expression induced primary cilia disassembly during palate development. Sonic hedgehog and Patched1 expression levels and palatine rugae morphology were altered in the over-expressed Pitchfork group during palate development. Thus, the proper expression levels of Pitchfork might play a pivotal role in normal secondary palate morphogenesis.
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