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Titolo:
Zebrafish colourless encodes sox10 and specifies non-ectomesenchymal neural crest fates
Autore:
Dutton, KA; Pauliny, A; Lopes, SS; Elworthy, S; Carney, TJ; Rauch, J; Geisler, R; Haffter, P; Kelsh, RN;
Indirizzi:
Univ Bath, Dept Biol & Biochem, Bath BA2 7AY, Avon, England Univ Bath Bath Avon England BA2 7AY Biochem, Bath BA2 7AY, Avon, England Max Planck Inst Entwicklungsbiol, D-72076 Tubingen, Germany Max Planck Inst Entwicklungsbiol Tubingen Germany D-72076 ingen, Germany
Titolo Testata:
DEVELOPMENT
fascicolo: 21, volume: 128, anno: 2001,
pagine: 4113 - 4125
SICI:
0950-1991(200111)128:21<4113:ZCESAS>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
WAARDENBURG-HIRSCHSPRUNG-DISEASE; ENDOTHELIN-B RECEPTOR; TRANSCRIPTION FACTOR; DANIO-RERIO; EMBRYONIC ZEBRAFISH; MOUSE MODEL; CELL FATE; GENE; EXPRESSION; MUTATION;
Keywords:
Danio rerio; Waardenburg-Shah syndrome; Hirschsprung's disease; pigment cells; melanophore; apoptosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Kelsh, RN Univ Bath, Dept Biol & Biochem, Claverton Down, Bath BA2 7AY, Avon, England Univ Bath Claverton Down Bath Avon England BA2 7AY Avon, England
Citazione:
K.A. Dutton et al., "Zebrafish colourless encodes sox10 and specifies non-ectomesenchymal neural crest fates", DEVELOPMENT, 128(21), 2001, pp. 4113-4125

Abstract

Waardenburg-Shah syndrome combines the reduced enteric nervous system characteristic of Hirschsprung's disease with reduced pigment cell number, although the cell biological basis of the disease is unclear. We have analysed a zebrafish Waardenburg-Shah syndrome model. We show that the colourless gene encodes a sox10 homologue, identify sox10 lesions in mutant alleles and rescue the mutant phenotype by ectopic sox10 expression. Using iontophoretic labelling of neural crest cells, we demonstrate that colourless mutant neural crest cells form ectomesenchymal fates. By contrast, neural crest cells which in wild types form non-ectomesenchymal fates generally fail to migrate and do not overtly differentiate. These cells die by apoptosis between 35 and 45 hours post fertilisation. We provide evidence that melanophore defects in colourless mutants can be largely explained by disruption of nacre/mitf expression. We propose that all defects of affected crest derivativesare consistent with a primary role for colourless/sox10 in specification of non-ectomesenchymal crest derivatives. This suggests a novel mechanism for the aetiology of Waardenburg-Shah syndrome in which affected neural crestderivatives fail to be generated from the neural crest.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/05/20 alle ore 14:52:25