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The ectodermal loss of ARHGAP29 alters epithelial morphology and disrupts murine palatogenesis
Journal article   Open access   Peer reviewed

The ectodermal loss of ARHGAP29 alters epithelial morphology and disrupts murine palatogenesis

Emily Adelizzi, Lindsey Rhea, Campbell Mitvalsky, Samuel Pek, Bethany Doolittle and Martine Dunnwald
Development (Cambridge), Vol.153(12), dev205636
06/2026
DOI: 10.1242/dev.205636
PMID: 42272439
Appears in  UI Libraries Support Open Access
url
https://doi.org/10.1242/dev.205636View
Published (Version of record) Open Access

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 mutations in 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 (E) day 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.
 Cleft Development ARHGAP29 Palatogenesis Mouse UIOWA OA Agreement

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