Linked Life Data

21074523

Source:http://linkedlifedata.com/resource/pubmed/id/21074523

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-1-10
pubmed:abstractText
For the correct development of the central nervous system, the balance between self-renewing and differentiating divisions of the neuronal progenitors must be tightly regulated. To maintain their self-renewing identity, the progenitors need to retain both apical and basal interfaces. However, the identities of fate-determining signals which cells receive via these connections, and the exact mechanism of their action, are poorly understood. The conditional inactivation of Fibroblast growth factor (FGF) receptors 1 and 2 in the embryonic mouse midbrain-hindbrain area results in premature neuronal differentiation. Here, we aim to elucidate the connection between FGF signaling and neuronal progenitor maintenance. Our results reveal that the loss of FGF signaling leads to downregulation of Hes1 and upregulation of Ngn2, Dll1, and p57 in the ventricular zone (VZ) cells, and that this increased neurogenesis occurs cell-autonomously. Yet the cell cycle progression, apico-basal-polarity, cell-cell connections, and the positioning of mitotic spindle in the mutant VZ appear unaltered. Interestingly, FGF8-protein is highly concentrated in the basal lamina. Thus, FGFs may act through basal processes of neuronal progenitors to maintain their progenitor status. Indeed, midbrain neuronal progenitors deprived in vitro of FGFs switched from symmetrical proliferative towards symmetrical neurogenic divisions. We suggest that FGF signaling in the midbrain VZ is cell-autonomously required for the maintenance of symmetrical proliferative divisions via Hes1-mediated repression of neurogenic genes.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1095-564X
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
349
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
270-82
pubmed:dateRevised
2011-9-14
pubmed:meshHeading
pubmed-meshheading:21074523-Animals, pubmed-meshheading:21074523-Basic Helix-Loop-Helix Transcription Factors, pubmed-meshheading:21074523-Bromodeoxyuridine, pubmed-meshheading:21074523-Cell Proliferation, pubmed-meshheading:21074523-Crosses, Genetic, pubmed-meshheading:21074523-Fibroblast Growth Factors, pubmed-meshheading:21074523-Gene Expression Regulation, Developmental, pubmed-meshheading:21074523-Homeodomain Proteins, pubmed-meshheading:21074523-Immunohistochemistry, pubmed-meshheading:21074523-In Situ Hybridization, pubmed-meshheading:21074523-Mesencephalon, pubmed-meshheading:21074523-Mice, pubmed-meshheading:21074523-Neural Stem Cells, pubmed-meshheading:21074523-Neurogenesis, pubmed-meshheading:21074523-Receptors, Fibroblast Growth Factor, pubmed-meshheading:21074523-Signal Transduction
pubmed:year
2011
pubmed:articleTitle
FGF signaling gradient maintains symmetrical proliferative divisions of midbrain neuronal progenitors.
pubmed:affiliation
Department of Biological and Environmental Sciences, University of Helsinki, 00014, Helsinki, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't