Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Inactivation of the beta-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development
Autore:
Brault, V; Moore, R; Kutsch, S; Ishibashi, M; Rowitch, DH; McMahon, AP; Sommer, L; Boussadia, O; Kemler, R;
Indirizzi:
Max Planck Inst Immunbiol, Dept Mol Embryol, D-79108 Freiburg, Germany MaxPlanck Inst Immunbiol Freiburg Germany D-79108 108 Freiburg, Germany Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA Harvard Univ Cambridge MA USA 02138 ellular Biol, Cambridge, MA 02138 USA ETH Honggerberg, Swiss Fed Inst Technol, Inst Cell Biol, CH-8093 Zurich, Switzerland ETH Honggerberg Zurich Switzerland CH-8093 , CH-8093 Zurich, Switzerland
Titolo Testata:
DEVELOPMENT
fascicolo: 8, volume: 128, anno: 2001,
pagine: 1253 - 1264
SICI:
0950-1991(200104)128:8<1253:IOTBGB>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
CRANIAL NEURAL CREST; CENTRAL-NERVOUS-SYSTEM; ADHESION MOLECULE UVOMORULIN; TRANSCRIPTION FACTOR AP-2; PROTO-ONCOGENE INT-1; ACID-BINDING-PROTEIN; MOUSE EMBRYO; CELL-MIGRATION; E-CADHERIN; MUTANT MICE;
Keywords:
beta-catenin; cell adhesion; Wnt1; conditional inactivation; CNS development; neural crest; mouse;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
96
Recensione:
Indirizzi per estratti:
Indirizzo: Kemler, R Max Planck Inst Immunbiol, Dept Mol Embryol, Stuebeweg 51, D-79108 Freiburg, Germany Max Planck Inst Immunbiol Stuebeweg 51 Freiburg Germany D-79108
Citazione:
V. Brault et al., "Inactivation of the beta-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development", DEVELOPMENT, 128(8), 2001, pp. 1253-1264

Abstract

beta -Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta -catenin during brain morphogenesis, by specifically inactivating the beta -catenin gene in the region of Wnt1 expression. To achieve this, mice with a conditional ('floxed') allele of beta -catenin with required exons banked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of Wnt1 regulatory sequences. beta -catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional Wnt1 knockout (Wnt1(-/-)), suggesting that Wnt1 acts through beta -catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack Wnt1, indicates a role for beta -catenin in the fate of neural crest cells. Analysis of neural tube explants shows that beta -catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial gangliaand in areas of prechondrogenic condensations, suggests that removal of beta -catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta -catenin in morphogenetic processes during brain and craniofacial development.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 20:02:58