NDLI: Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling down syndrome

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Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling down syndrome

Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn

Erratum to: Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn

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Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling down syndrome

Content Provider	Springer Nature Link
Author	Duchon, Arnaud Raveau, Matthieu Chevalier, Claire Nalesso, Valérie Sharp, Andrew J. Herault, Yann
Copyright Year	2011
Abstract	Down syndrome (DS) is the most frequent genetic disorder leading to intellectual disabilities and is caused by three copies of human chromosome 21. Mouse models are widely used to better understand the physiopathology in DS or to test new therapeutic approaches. The older and the most widely used mouse models are the trisomic Ts65Dn and the Ts1Cje mice. They display deficits similar to those observed in DS people, such as those in behavior and cognition or in neuronal abnormalities. The Ts65Dn model is currently used for further therapeutic assessment of candidate drugs. In both models, the trisomy was induced by reciprocal chromosomal translocations that were not further characterized. Using a comparative genomic approach, we have been able to locate precisely the translocation breakpoint in these two models and we took advantage of this finding to derive a new and more efficient Ts65Dn genotyping strategy. Furthermore, we found that the translocations introduce additional aneuploidy in both models, with a monosomy of seven genes in the most telomeric part of mouse chromosome 12 in the Ts1Cje and a trisomy of 60 centromeric genes on mouse chromosome 17 in the Ts65Dn. Finally, we report here the overexpression of the newly found aneuploid genes in the Ts65Dn heart and we discuss their potential impact on the validity of the DS model.
Starting Page	674
Ending Page	684
Page Count	11
File Format	PDF
ISSN	09388990
Journal	Mammalian Genome
Volume Number	22
Issue Number	11-12
e-ISSN	14321777
Language	English
Publisher	Springer-Verlag
Publisher Date	2011-09-28
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Zoology Cell Biology Anatomy
Content Type	Text
Resource Type	Article
Subject	Genetics

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Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling down syndrome

Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling down syndrome

Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn

Postnatal lethality and cardiac anomalies in the Ts65Dn Down Syndrome mouse model

Erratum to: Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn

Molecular Characterization of the Translocation Breakpoints in the Down Syndrome Mouse Model, Ts65Dn

Increased male reproductive success in Ts65Dn “Down syndrome” mice

Molecular responses of the Ts65Dn and Ts1Cje mouse models of Down syndrome to MK-801

Functional transcriptome analysis of the postnatal brain of the Ts1Cje mouse model for Down syndrome reveals global disruption of interferon-related molecular networks

Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling down syndrome

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Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling down syndrome