Document Detail


Altered signaling pathway in the dysmorphogenesis of telencephalon in the Gli3 depressed mouse embryo, Pdn/Pdn.
MedLine Citation:
PMID:  18452488     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The responsible gene of genetic polydactyly/arhinencephaly mouse (Pdn/Pdn) is Gli3. Pdn/Pdn exhibits absence of the olfactory bulb, suggesting telencephalic dysmorphogenesis. It has been cleared that a transposon was inserted into intron 3 of the Gli3 gene in the Pdn mouse. Adequate PCR primers in the intron 3 and transposon allowed us to discriminate +/+, Pdn/+ and Pdn/Pdn embryos. After genotyping of the Pdn embryos using genomic DNA from the yolk sac membrane, gene expressions in the embryo proper were analyzed by DNA microarray, real-time PCR and whole-mount in situ hybridization (WISH) methods. DNA microarray detected 368 depressed and 425 over-expressed genes in the Pdn/Pdn mouse embryos on day 9 of gestation. In these genes, six signaling pathway and 20 transcription factor genes were included. From these genes, we further investigated Gli3, Emx2, Wnt8b and Wnt7b gene expressions using real-time PCR and WISH, and depression of these gene expression amounts and altered expression patterns were confirmed. Although alterations of Shh and Fgf8 gene expressions were not detected in the DNA microarray, as these genes have been closed up in the telencephalic morphogenesis, we investigated these gene expressions by real-time PCR and WISH. Shh gene expression amount and pattern were not changed. Alteration of Fgf8 gene expression amount was not detected also in the real-time PCR, but altered expression pattern was detected in the Pdn/Pdn embryos by WISH. From the present data, we suggested that Emx2, Wnt8b, Wnt7b and Fgf8 are the important Gli3 signaling pathway in the morphogenesis of telencephalon.
Authors:
Etsuko Ueta; Maho Kurome; Yuko Teshima; Mami Kodama; Yuzuru Otsuka; Ichiro Naruse
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Congenital anomalies     Volume:  48     ISSN:  0914-3505     ISO Abbreviation:  Congenit Anom (Kyoto)     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-05-02     Completed Date:  2008-08-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9306292     Medline TA:  Congenit Anom (Kyoto)     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  74-80     Citation Subset:  IM    
Affiliation:
School of Health Science, Faculty of Medicine, Tottori University, Yonago, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
In Situ Hybridization
Kruppel-Like Transcription Factors / genetics,  physiology*
Mice
Mice, Inbred ICR
Morphogenesis
Nerve Tissue Proteins / genetics,  physiology*
Oligonucleotide Array Sequence Analysis
Polymerase Chain Reaction
Signal Transduction*
Telencephalon / abnormalities,  embryology*,  metabolism
Chemical
Reg. No./Substance:
0/Gli3 protein, mouse; 0/Kruppel-Like Transcription Factors; 0/Nerve Tissue Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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