Linked Life Data

20674670

Source:http://linkedlifedata.com/resource/pubmed/id/20674670

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-9-20
pubmed:abstractText
Neuronal apoptosis sculpts the developing brain, and nearly all identified classes of neurons seem to be produced "in excess" during development. FoxO transcription factors regulate apoptosis in vitro in deprived of neurotrophins. It is unknown if FoxO3a is involved in the development of neurons. Here, we report a role of FoxO3a during neuronal development in zebrafish. By using in situ hybridization, we revealed that FoxO3a transcripts in zebrafish were gradually confined to regions of the central nervous system during embryonic development, including the forebrain, midbrain, midbrain-hindbrain boundary and hindbrain. By using FoxO3a morpholino antisense oligonucleotides, we observed that FoxO3a loss-of-function led to neural developmental defects, including increased neural apoptosis as detected by acridine orange and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling. These defects could be partially rescued by the injection of FoxO3a mRNA. In this study, we found that FoxO3a loss-of-function resulted in the decreased expression of neuronal markers as determined by in situ hybridization and relative quantitative real-time PCR. Furthermore, the activation of FoxO3a was required for the maintenance of neuron survival but not necessary for the induction of neurogenesis. Our results indicated that FoxO3a might be essential for the maintenance of neural development in zebrafish. Therefore, this work provides novel evidence of FoxO3a in the embryonic neurodevelopment from zebrafish to other mammals.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1872-7972
pubmed:author
pubmed:copyrightInfo
Crown Copyright © 2010. Published by Elsevier Ireland Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
29
pubmed:volume
484
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
98-103
pubmed:dateRevised
2011-2-4
pubmed:meshHeading
pubmed-meshheading:20674670-Amino Acid Sequence, pubmed-meshheading:20674670-Animals, pubmed-meshheading:20674670-Animals, Genetically Modified, pubmed-meshheading:20674670-Apoptosis, pubmed-meshheading:20674670-Brain, pubmed-meshheading:20674670-Embryo, Nonmammalian, pubmed-meshheading:20674670-Embryonic Development, pubmed-meshheading:20674670-Forkhead Transcription Factors, pubmed-meshheading:20674670-Gene Expression Regulation, Developmental, pubmed-meshheading:20674670-Gene Knockdown Techniques, pubmed-meshheading:20674670-Green Fluorescent Proteins, pubmed-meshheading:20674670-Nerve Tissue Proteins, pubmed-meshheading:20674670-Neural Cell Adhesion Molecules, pubmed-meshheading:20674670-Neurons, pubmed-meshheading:20674670-Oligonucleotides, Antisense, pubmed-meshheading:20674670-RNA, Messenger, pubmed-meshheading:20674670-Superoxide Dismutase, pubmed-meshheading:20674670-Zebrafish, pubmed-meshheading:20674670-Zebrafish Proteins
pubmed:year
2010
pubmed:articleTitle
Knockdown of FoxO3a induces increased neuronal apoptosis during embryonic development in zebrafish.
pubmed:affiliation
Laboratory of Integrated Bioscience, School of Life Science, Sun Yat-sen University, No. 135 West XinGang Road, Guangzhou 510275, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't