ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2014
Embryonic expression of EphA receptor genes in mice supports their candidacy for involvement in cleft lip and palate.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- EphA4 Mediates EphrinB1-Dependent Adhesion in Retinal Ganglion Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- 3D facial phenotyping by biometric sibling matching used in contemporary genomic methodologies.PLoS genetics · 2021Article
- Aberrant cell segregation in the craniofacial primordium and the emergence of facial dysmorphology in craniofrontonasal syndrome.PLoS genetics · 2020Article
- Cellular organization and boundary formation in craniofacial development.Genesis (New York, N.Y. : 2000) · 2019Review
- Closing the Gap: Mouse Models to Study Adhesion in Secondary Palatogenesis.Journal of dental research · 2017Review
- Ephrin Ligands and Eph Receptors Show Regionally Restricted Expression in the Developing Palate and Tongue.Frontiers in physiology · 2016Article
- The putative tumor suppressor gene EphA3 fails to demonstrate a crucial role in murine lung tumorigenesis or morphogenesis.Disease models & mechanisms · 2015Article
- Quantitative trait loci affecting the 3D skull shape and size in mouse and prioritization of candidate genes in-silico.Frontiers in physiology · 2015Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundEph receptors, comprising the A- and B-subfamilies, are the largest family of receptor tyrosine kinases in the mammalian genome, and their function is critical for morphogenesis in a variety of contexts. Whereas signaling through B-type Ephs has been demonstrated to play a role in cleft lip and palate (CL/P), the involvement of A-type Ephs has not been examined in this context notwithstanding a recent genome-wide association study that identified the EPHA3 locus as a candidate for non-syndromic CL/P.
resultsHere, we present a systematic analysis of the gene expression patterns for the nine EphA receptors at progressive stages of mouse development and find that EphA3, EphA4, and EphA7 exhibit restricted overlapping patterns of expression during palate development. We find that homozygous mutation of EphA3 or compound homozygous mutation of EphA3 and EphA4 in mice does not result in defective midfacial development, supporting the possibility of redundant function with EphA7. We also document previously undescribed expression patterns in other tissues of the craniofacial complex including the lacrimal duct and salivary glands.
conclusionsTogether, these results are consistent with the hypothesis that mutations in EPHA family genes may cause CL/P and also suggest that functional redundancy between family members may be at play.
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