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Interaction of endothelin-3 with endothelin-B receptor is essential for development of epidermal melanocytes and enteric neurons.

Abstract：

:Defects in the gene encoding the endothelin-B receptor produce aganglionic megacolon and pigmentary disorders in mice and humans. We report that a targeted disruption of the mouse endothelin-3 ligand (EDN3) gene produces a similar recessive phenotype of megacolon and coat color spotting. A natural recessive mutation that results in the same developmental defects in mice, lethal spotting (ls), failed to complement the targeted EDN3 allele. The ls mice carry a point mutation of the EDN3 gene, which replaces the Arg residue at the C-terminus of the inactive intermediate big EDN3 with a Trp residue. This mutation prevents the proteolytic activation of big EDN3 by ECE-1. These findings indicate that interaction of EDN3 with the endothelin-B receptor is essential in the development of neural crest-derived cell lineages. We postulate that defects in the human EDN3 gene may cause Hirschsprung's disease.

journal_name

Cell

journal_title

Cell

authors

Baynash AG,Hosoda K,Giaid A,Richardson JA,Emoto N,Hammer RE,Yanagisawa M

doi

10.1016/0092-8674(94)90018-3

subject

Has Abstract

pub_date

1994-12-30 00:00:00

pages

1277-85

issue

7

eissn

0092-8674

issn

1097-4172

pii

0092-8674(94)90018-3

journal_volume

79

pub_type

杂志文章

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