Linked Life Data

19842188

Source:http://linkedlifedata.com/resource/pubmed/id/19842188

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-12-24
pubmed:abstractText
Wnt/beta-catenin signaling controls the proper development of the mid-/hindbrain region (MHR) and of midbrain dopaminergic (mDA) neurons, but the Frizzled (Fzd) receptors transducing these signals are still unknown. Fzd3 is expressed throughout the mouse anterior neural tube, whereas Fzd6 is restricted to the MHR. We show that the MHR is properly established and mDA neurons develop normally in Fzd6(-/-) mutants, but the number of mDA neurons is initially reduced and recovers at later stages in Fzd3(-/-) embryos. Fzd3(-/-); Fzd6(-/-) double mutants exhibit a severe midbrain morphogenesis defect consisting of collapsed brain ventricles, apparent thickening of the neuroepithelium, focal disruption of the ventricular basal lamina and protrusion of individual cells, and increased proliferation at later stages, despite a normal closure of the anterior neural tube and the rescue of the mDA defect in these embryos. Fzd3 and Fzd6 thus control proper midbrain morphogenesis by a yet unknown mechanism in the mouse.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1097-0177
pubmed:author
pubmed:copyrightInfo
(c) 2009 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
239
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
246-60
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Fzd3 and Fzd6 deficiency results in a severe midbrain morphogenesis defect.
pubmed:affiliation
Institute of Developmental Genetics, Helmholtz Centre Munich, German Research Centre for Environmental Health, and Technical University Munich, Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Munich/Neuherberg, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't