ArticleDevelopment (Cambridge, England)2026
Ectodermal loss of ARHGAP29 alters epithelial morphology and disrupts murine palatogenesis.
Article in Development (Cambridge, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Orofacial clefts, including cleft palate (CP), are among the most common types of birth defects. CP results from a failure of palatal shelf fusion during development. Previous human studies have shown that variants of the RhoA GTPase activating protein 29 (ARHGAP29) gene are linked to CP, yet the role and tissue-specific requirements for ARHGAP29 during palatogenesis remain unknown. Here, we use tissue-specific deletion of Arhgap29 in mice to provide the first direct evidence that ARHGAP29 is essential for palatal elevation and fusion. We demonstrate that ectodermal conditional loss of Arhgap29 induces a significant delay in palatogenesis at embryonic day (E) 14.5 and a significant, complete cleft of the secondary palate at E18.5, which is not observed when Arhgap29 is lost later in development using K14-Cre and K6-Cre. Phenotypic analyses of palatal shelves at E14.5 reveal a disorganized and thicker epithelium. Loss of Arhgap29 increases palatal epithelial cell area and upregulates markers of contractility including alpha-smooth muscle actin and phospho-myosin regulatory light chain, implicating cell morphology and contractility as potential drivers of CP.
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