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Gene expression signature of cerebellum hypoplasia in a mouse model of Down syndrome (Part I).

ABSTRACT: We designed a large scale gene expression study in Ts1Cje mice between P0 and P10 in order to measure the effects of trisomy 21 on a large number of samples (56 in total) in a tissue that is affected in Down syndrome (the cerebellum) and to quantify the defect during development in order to correlate gene expression changes to the phenotype observed. Keywords: Down syndrome, Ts1Cje, cerebellum, development, hypoplasia

ORGANISM(S): Mus musculus

PROVIDER: GSE11448 | GEO | 2009/03/31

SECONDARY ACCESSION(S): PRJNA106479

REPOSITORIES: GEO

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Gene expression signature of cerebellum hypoplasia in a mouse model of Down syndrome (Part I).

Project description:We designed a large scale gene expression study in Ts1Cje mice between P0 and P10 in order to measure the effects of trisomy 21 on a large number of samples (56 in total) in a tissue that is affected in Down syndrome (the cerebellum) and to quantify the defect during development in order to correlate gene expression changes to the phenotype observed. Keywords: Down syndrome, Ts1Cje, cerebellum, development, hypoplasia We analyzed gene expression in the cerebellum of Ts1Cje and euploid mice at P0, P3, P7 and P10 using pangenomic two colors microarrays containing 25 344 probes representing approximately 15 574 mouse genes. 56 samples from individual cerebellum were hybridized on 28 microarrays. On each microarray we hybridized a Ts1Cje sample versus an euploid sample and always a male versus a female. In addition on the same microarray we always compared samples from mice of the same age or with a maximum difference of 4 days (P0 versus P3, P3 versus P7 or P7 versus P10).

2009-03-31 | E-GEOD-11448 | biostudies-arrayexpress

Gene expression signature of cerebellum hypoplasia in a mouse model of Down syndrome (Part II).

2008-03-31 | GSE11472 | GEO

Gene expression signature of cerebellum hypoplasia in a mouse model of Down syndrome (Part II).

Project description:We designed a large scale gene expression study in cerebellar external granular layer in Ts1Cje mice at P0 in order to measure the effects of trisomy 21 on in a enriched cell population (dissected layer) that is affected in Down syndrome in order to correlate gene expression changes to the phenotype observed. Keywords: Down syndrome, Ts1Cje, EGL, hypoplasia We analyzed gene expression in the EGL of Ts1Cje and euploid mice at P0 using pangenomic Illumina mouse-6 v1.1 expression beadchips containing 46 632 probes representing approximately 19 000 mouse genes. 18 samples from individual cerebellar EGL were hybridized on 18 microarrays (6 by slide). On each slide, we hybridized 6 samples frome the same litter.

2008-03-31 | E-GEOD-11472 | biostudies-arrayexpress

Transcriptome of Ts1Cje and euploids cerebellum

Project description:Transcriptome analysis of Ts1Cje (mouse model of Down syndrome) and euploids murine cerebellum during postnatal development Keywords = Down syndrome Keywords = Chromosome 21 Keywords = Transcriptome Keywords = Microarray Keywords = Cerebellum Keywords = Development Keywords: other

2004-12-05 | GSE1611 | GEO

Transcription profiling by array of mouse Ts1Cje (mouse model of Down syndrome) and euploids murine cerebellum during postnatal development

2004-12-05 | E-GEOD-1611 | biostudies-arrayexpress

Biomarkers for Down Syndrome screening in murine fetal liver and placenta

Project description:The Ts1Cje mouse strain (Sago, 1998) contains a segmental trisomy of mouse chromosome 16 orthologous to the region of human chromosome 21 commonly associated with Down Syndrome. In this study, fetuses were obtained from wildtype mothers bred with either wildtype or Ts1Cje males. Gene expression profiles in fetal liver and placenta of wildtype and Ts1Cje fetuses were compared, to identify potential markers for application in human prenatal DS screening.

2011-05-11 | GSE24272 | GEO

Delayed cell cycling in DS Ts1Cje neural precursor cells results in gene expression dysregulation

Project description:Down syndrome neurophenotypes are characterized by mental retardation and a decreased brain volume. In order to identify whether deficits in proliferation, differentiation or survival could be responsible for this phenotype, neural precursor cells (NPCs) were isolated from the developing E14 neocortex of Down syndrome partial trisomy Ts1Cje mice and euploid (WT) littermates. Proliferation, cell differentiation and cell death assays revealed that Ts1Cje NPCs proliferated at a slower rate, due to a longer cell cycle and that a greater number of cells were positive for glial fibrillary acidic protein. An increase in Ts1Cje NPC cell death was also noted. Gene expression profiling was conducted on RNA extracted from Ts1Cje and WT NPCs. Approximately 54% of triploid gene expression ratios were significantly greater than the expected diploid gene ratio of 1.0. A number of diploid genes associated with differentiation, glial function and proliferation were dysregulated. The evidence points to a delay in cellular cycling that could exert stress on the NPC population, which might result in cellular death and a mobilization of glial cell survival responses. Importantly, these phenotypic changes, which mimic those seen in Down syndrome individuals, do not require over-expression of amyloid precursor protein (App) or soluble superoxide dismutase 1 (Sod1). In conclusion, early developmental proliferation deficits in Down syndrome result in secondary morphological changes that can impact on cognitive development and function. Keywords: Down syndrome, Neocortical precursor cells, transcriptome, proliferation Neural precursor cells (NPCs) were isolated from mouse E14 neocortex of Down syndrome Ts1Cje mice and euploid littermates. We compared gene expression profiles from trisomic and wild-type cells using pangenomic microarrays.

2010-05-19 | E-GEOD-9805 | biostudies-arrayexpress

Delayed cell cycling in DS Ts1Cje neural precursor cells results in gene expression dysregulation

2009-04-30 | GSE9805 | GEO

Expression data from Ts1Cje and disomic C57BL/6 adult neurospheres

Project description:Down syndrome is the most common form of genetic mental retardation. How Trisomy 21 causes mental retardation remains unclear and its effects on adult neurogenesis have not been addressed. To gain insight into the mechanisms causing mental retardation we used microarrays to investigate gene expression differences between Ts1Cje (a mouse model of Down syndrome) and C57BL/6 littermate control neurospheres. The neurospheres were generated from neural stem cells and progenitors isolated from the lateral walls of the lateral ventricles from adult mice. RNA was extracted for hybridization to arrays from 3 pairs of Ts1Cje and disomic C57BL/6 littermate control 7-day old adult neurosphere cultures.

2010-07-16 | E-GEOD-17760 | biostudies-arrayexpress

Trisomy 21 and TS13

Project description:Gene expression was measured in trisomy 21 and trisomy 13 human fetal samples. For TS21, regions assayed were cerebrum, cerebellum, heart, and cerebrum-derived astrocyte cell lines. Keywords = trisomy 21 Keywords = Down syndrome Keywords = aneuploidy Keywords = brain Keywords = heart Keywords = trisomy 13 Keywords: other

2005-05-10 | GSE1397 | GEO

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