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is required for cardiovascular development and interacts with in the pharyngeal endoderm to control 4th pharyngeal arch artery morphogenesis. | LitMetric

Developmental defects affecting the heart and aortic arch arteries are a significant phenotype observed in individuals with 22q11 deletion syndrome and are caused by a microdeletion on chromosome 22q11. , one of the deleted genes, is expressed throughout the pharyngeal arches and is considered a key gene, when mutated, for the arch artery defects. is expressed in the pharyngeal endoderm and is downregulated in mutant mice. We show here that -deficient mice are born with complex cardiovascular malformations that affect the outflow tract and aortic arch arteries with failure of the 3rd and 4th pharyngeal arch arteries to form correctly. Transcriptome analysis indicated that and may function together, and mice double heterozygous for / presented with a significantly increased incidence of interrupted aortic arch when compared with heterozygous mice. Using a novel allele, we demonstrated that the site of this genetic interaction is the pharyngeal endoderm, therefore revealing that a --controlled signalling mechanism emanating from the pharyngeal endoderm is required for crucial tissue interactions during normal morphogenesis of the pharyngeal arch artery system.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6765178PMC
http://dx.doi.org/10.1242/dev.177618DOI Listing

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