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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Julien Laffaire

PROVIDER: E-GEOD-11472 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression signature of cerebellar hypoplasia in a mouse model of Down syndrome during postnatal development.

Laffaire Julien J Rivals Isabelle I Dauphinot Luce L Pasteau Fabien F Wehrle Rosine R Larrat Benoit B Vitalis Tania T Moldrich Randal X RX Rossier Jean J Sinkus Ralph R Herault Yann Y Dusart Isabelle I Potier Marie-Claude MC

BMC genomics 20090330

<h4>Background</h4>Down syndrome is a chromosomal disorder caused by the presence of three copies of chromosome 21. The mechanisms by which this aneuploidy produces the complex and variable phenotype observed in people with Down syndrome are still under discussion. Recent studies have demonstrated an increased transcript level of the three-copy genes with some dosage compensation or amplification for a subset of them. The impact of this gene dosage effect on the whole transcriptome is still deba ...[more]

PMID: 19331679

Similar Datasets

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

2008-03-31 | GSE11472 | 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

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

2009-03-31 | GSE11448 | GEO

DNA microarray analysis using murine cerebellum at P6

Project description:We analysed genes upregulated or down regulated by double deletion of Rac1 and Rac3 (Rac1/Rac3-DKO) in cerebellar granule neurons compared with control, using the external granule layer (EGL) dissected from Rac1/Rac3-DKO cerebellum at P6. Rac1-KO mouse is an inducible knockout, in which Rac1 is specifically deleted in cerebellar granule neurons under control of Atoh1 (also called Math1) promoter. In contrast, Rac3-KO mouse is a conventional/simple KO, in which Rac3 is deleted in all cells in the body. Total RNA from the medial portion of the EGL of Rac1/Rac3-DKO and control cerebella at P6 was extracted using TRIzol (Invitrogen). The quality and quantity of RNA were determined using the Agilent 2100 BioAnalyzer.

2017-05-16 | E-MTAB-5681 | biostudies-arrayexpress

The identification and tumorigenecity of neuronal progenitors in developing cerebellum

Project description:It is generally believed that cerebellar granule neurons originate exclusively from granule neuron precursors (GNPs) in the external germinal layer (EGL). Here we identify a rare population of neuronal progenitors in the developing cerebellum that expresses Nestin. Although Nestin is widely considered a marker for multipotent stem cells, these Nestin-expressing progenitors (NEPs) are committed to the granule neuron lineage. Unlike conventional GNPs, which reside in the outer EGL and proliferate extensively, NEPs reside in the deep part of the EGL and are quiescent. Expression profiling reveals that NEPs are distinct from GNPs, and in particular, express markedly reduced levels of genes associated with DNA repair. Consistent with this, upon aberrant activation of Sonic hedgehog (Shh) signaling, NEPs exhibit more severe genomic instability and give rise to tumors more efficiently than GNPs. These studies identify a novel progenitor for cerebellar granule neurons and a novel cell of origin for medulloblastoma.

2013-09-13 | GSE50824 | GEO

The identification and tumorigenecity of neuronal progenitors in developing cerebellum

2013-09-13 | E-GEOD-50824 | biostudies-arrayexpress

Transcription profiling of rat cerebellar granular cells cultured in the presence of Shh for 24h and then pulsed with Bmp2 or vehicle for up to 24h

Project description:Proliferating cerebellar granular cells were cultured in presence of Shh for 24h (3ug/ml) and then pulsed for additional 24h with Bmp2 or vehicle. Cells then were lysed and mRNA extracted. Microarray data from cells treated with Bmp2 was referred to the control not treated with Bmp2.

2007-06-07 | E-MEXP-1129 | 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

Apical complex protein Pals1 is required to maintain cerebellar progenitor cells in a proliferative state

Project description:Through their biased localization and function within the cell, polarity complex proteins are necessary to establish the cellular asymmetry required for tissue organization. Well-characterized germinal zones, mitogenic signals, and cell types make the cerebellum an excellent model for addressing the critical function of polarity complex proteins in the generation and organization of neural tissues. Deleting apical polarity complex protein Pals1 in the developing cerebellum results in a remarkably undersized cerebellum with disrupted layers in poorly formed folia and strikingly reduced granule cell production. We demonstrate that Pals1 is not only essential for cerebellum organogenesis, but also for preventing premature differentiation and thus maintaining progenitor pools in cerebellar germinal zones, including cerebellar granule neuron precursors (CGNP) in the external granule layer (EGL). In the Pals1 mutants, expression of genes that regulate cell cycle were diminished, correlating with the loss of proliferating population of germinal zones. Furthermore, enhanced Shh signaling through activated Smoothened (Smo) cannot overcome impaired cerebellar cell generation, arguing for an epistatic role of Pals1 in proliferation capacity. Our study identifies Pals1 as a new intrinsic factor that regulates the generation of cerebellar cells and Pals1 deficiency as a potential inhibitor of overactive mitogenic signaling. Two groups of samples are included: mRNA obtained from 4 WT and 4 CKO animals at E17.5. hGFAP-Cre mice was used to delete Pals1 from most cerebellar neurons and glia (termed Pals1 CKO). Pals1fl/fl and hGFAP-Cre (Zhuo et al., 2001) were bred for generation of CKO.

2016-06-30 | E-GEOD-75696 | biostudies-arrayexpress

Expression data from 3-month-old mouse hippocampus 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 in hippocampus at 3-month-old . We analyzed the effect of Ts1Cje trisomic region on global gene expression in the adult brain of Ts1Cje mice at 3-month-old.

2021-08-01 | GSE160185 | GEO

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