Neural crest defects in ephrin-B2 mutant mice are non-autonomous and originate from defects in the vasculature.

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.

journal_name

Dev Biol

journal_title

Developmental biology

authors

Lewis AE,Hwa J,Wang R,Soriano P,Bush JO

doi

10.1016/j.ydbio.2015.08.021

subject

Has Abstract

pub_date

2015-10-15 00:00:00

pages

186-95

issue

2

eissn

0012-1606

issn

1095-564X

pii

S0012-1606(15)30154-8

journal_volume

406

pub_type

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