ArticleFrontiers in cell and developmental biology2026
TCF4 at the crest of development: a zebrafish model to explore craniofacial and gastrointestinal defects in Pitt-Hopkins syndrome.
Article in Frontiers in cell and developmental biology, 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
Background: Pitt-Hopkins Syndrome (PTHS) is a rare neurodevelopmental disorder caused by haploinsufficiency of the Methods: We generated a zebrafish Results: Heterozygous mutants exhibit key features of PTHS, including craniofacial skeletal abnormalities and impaired gastrointestinal motility. Functional analysis revealed a significant reduction of spontaneous peristaltic contractions and a delayed swallow-induced gut transit, consistently with human patients and PTHS mouse model. To further elucidate these developmental alterations, we showed that these defects are associated with a reduced number of Phox2b-positive enteric progenitors and HuC-positive enteric neurons, though early vagal neural crest migration appears unaffected. Reintroducing human TCF4 mRNA in tcf4 heterozygous mutant embryos rescues both craniofacial and gastrointestinal phenotypes, confirming the specificity of the observed phenotypes. Furthermore, we showed that the human Conclusion: Together, our results shed light on TCF4 as a key regulator of neural crest-derived lineages and provide a new perspective on two major clinical features of PTHS. The
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