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

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Luce Dauphinot

PROVIDER: E-GEOD-1611 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The cerebellar transcriptome during postnatal development of the Ts1Cje mouse, a segmental trisomy model for Down syndrome.

Dauphinot L L Lyle R R Rivals I I Dang M Tran MT Moldrich R X RX Golfier G G Ettwiller L L Toyama K K Rossier J J Personnaz L L Antonarakis S E SE Epstein C J CJ Sinet P-M PM Potier M-C MC

Human molecular genetics 20041208 3

The central nervous system of persons with Down syndrome presents cytoarchitectural abnormalities that likely result from gene-dosage effects affecting the expression of key developmental genes. To test this hypothesis, we have investigated the transcriptome of the cerebellum of the Ts1Cje mouse model of Down syndrome during postnatal development using microarrays and quantitative PCR (qPCR). Genes present in three copies were consistently overexpressed, with a mean ratio relative to euploid of ...[more]

PMID: 15590701

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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

Expression data from postnatal mouse brain regions of Ts1Cje and disomic C57BL/6 mice.

Project description:The Ts1Cje mouse model of Down syndrome (DS) has partial triplication of mouse chromosome 16 (MMU16), which is partially homologous to human chromosome 21. The mouse model develops various neuropathological features identified in DS individuals. We analysed the effect of partial triplication of the MMU16 segment on global gene expression in the cerebral cortex, cerebellum and hippocampus of Ts1Cje mice at 4 time-points; postnatal day (P)1, P15, P30 and P84. RNA was extracted from thre brain regions (Cerebral cortex, hippocampus and cerebellum) for hybridization to arrays from 3 pairs of Ts1Cje and disomic C57BL/6 littermate control for each timepoints at postnatal (P) day 1, P15, P30 and P84.

2014-07-23 | E-GEOD-49050 | biostudies-arrayexpress

Expression data from postnatal mouse brain regions of Ts1Cje and disomic C57BL/6 mice.

2014-07-23 | GSE49050 | GEO

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

2009-03-31 | GSE11448 | GEO

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

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

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

Expression data from E14.5 mouse brain regions of Ts1Cje and wild-type mice

Project description:The Ts1Cje mouse model of Down syndrome (DS) has partial triplication of mouse chromosome 16, of which a large portion is homologous to human chromosome 21. The mouse model shows an impaired neurogenesis at E14.5. We analyzed the effect of Ts1Cje trisomic region on global gene expression in the embryonic brain of Ts1Cje mice at E14.5.

2019-10-18 | GSE121449 | GEO

Expression data from skeletal muscles of Ts1Cje and disomic C57BL/6 mice

Project description:To determine the gene expression profile of extensor digitorum longus (EDL) and soleus (SO) muscles of wild-type and Ts1Cje mouse model of Down Syndrome (DS). Two types of skeletal muscles (EDL and SO) were harvested from both Ts1Cje and its disomic littermate.

2018-09-06 | GSE96572 | GEO

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

2009-04-30 | GSE9805 | GEO