ArticleDevelopmental biology2015
Neural crest defects in ephrin-B2 mutant mice are non-autonomous and originate from defects in the vasculature.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Disrupted endosomal trafficking of the Vangl-Celsr polarity complex underlies congenital anomalies in Xenopus trachea-esophageal morphogenesis.Developmental cell · 2025Article
- Evaluating neural crest cell migration in a Col4a1 mutant mouse model of ocular anterior segment dysgenesis.Cells & development · 2024Article
- Cellular and molecular mechanisms of the organogenesis and development, and function of the mammalian parathyroid gland.Cell and tissue research · 2023Review
- Tracheal separation is driven by NKX2-1-mediated repression of Efnb2 and regulation of endodermal cell sorting.Cell reports · 2022Article
- Endothelial cells during craniofacial development: Populating and patterning the head.Frontiers in bioengineering and biotechnology · 2022Review
- EphrinB2-EphB4-RASA1 Signaling in Human Cerebrovascular Development and Disease.Trends in molecular medicine · 2019Review
- Getting direction(s): The Eph/ephrin signaling system in cell positioning.Developmental biology · 2019Review
- Cellular organization and boundary formation in craniofacial development.Genesis (New York, N.Y. : 2000) · 2019Review
- Diabetic Ephrin-B2-Stimulated Peripheral Blood Mononuclear Cells Enhance Poststroke Recovery in Mice.Stem cells international · 2018Article
- Article
- An Ephrin-Eph Tug and Push in Left-Right Organ Placement.Developmental cell · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Ephrin-B2, a member of the Eph/ephrin family of cell signaling molecules, has been implicated in the guidance of cranial and trunk neural crest cells (NCC) and development of the branchial arches(BA), but detailed examination in mice has been hindered by embryonic lethality of Efnb2 null loss of function due to a requirement in angiogenic remodeling. To elucidate the developmental roles for Efnb2, we generated a conditional rescue knock-in allele that allows rescue of ephrin-B2 specifically in the vascular endothelium (VE), but is otherwise ephrin-B2 deficient. Restoration of ephrin-B2 expression specifically to the VE completely circumvents angiogenic phenotypes, indicating that the requirement of ephrin-B2 in angiogenesis is limited to the VE. Surprisingly, we find that expression of ephrin-B2 specifically in the VE is also sufficient for normal NCC migration and that conversely, embryos in which ephrin-B2 is absent specifically from the VE exhibit NCC migration and survival defects. Disruption of vascular development independent of loss of ephrin-B2 function also leads to defects in NCC and BA development. Together, these data indicate that direct ephrin-B2 signaling to NCCs is not required for NCC guidance, which instead depends on proper organization of the embryonic vasculature.
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