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Zebrafish notch signalling pathway mutants exhibit trunk vessel patterning anomalies that are secondary to somite misregulation
Author(s) -
Therapontos Christina,
Vargesson Neil
Publication year - 2010
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22410
Subject(s) - biology , notch signaling pathway , somitogenesis , somite , microbiology and biotechnology , filopodia , zebrafish , mutant , neurogenesis , ectopic expression , phenotype , anatomy , signal transduction , genetics , embryo , embryogenesis , actin , gene
The Notch signalling pathway mutants, after‐eight ( aei ), beamter ( bea ), and deadly‐seven ( des ) have previously been used to study somitogenesis and neurogenesis. Notch signalling has also been shown to have roles in vascular development. However, vascular development in each of these three Notch mutants has not been described, and so their potential usefulness for further understanding the role of Notch signalling in angiogenesis is unknown. Here we demonstrate each of the mutants also exhibit vascular defects in inter‐somitic vessel (ISV) positioning and patterning. Ectopic filopodia were also observed on the ISVs of the mutants. Ectopic filopodia are not due to loss of dll4 . Somite expression of known vascular guidance cues, efnb2, sema3a2 , and plexinD1 are disrupted, suggesting that the ISV vascular phenotype is due to disruption of these cues. Developmental Dynamics 239:2761–2768, 2010. © 2010 Wiley‐Liss, Inc.