Gene expression signature of cerebellum hypoplasia in a mouse model of Down syndrome (Part II).
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE11472 | GEO | 2008/03/31
SECONDARY ACCESSION(S): PRJNA106397
REPOSITORIES: GEO
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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
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
2009-03-31 | GSE11448 | GEO
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
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
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
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
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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
Project description:Down syndrome (DS) is caused by trisomy of chromosome 21 and it predisposes to hematological disorders such as transient myeloproliferative disorder and acute megakaryocytic leukemia. Our previous study identified a gain-of-function mutation of TRIB1 encoding a pseudokinase that suppresses C/EBP and enhances MEK/ERK signaling. In this study, we aimed to examine whether Trib1 expression cooperates with trisomy 21 in the development of leukemia. The wild type or R107L mutant Trib1 was retrovirally introduced into bone marrow cells derived from the Ts1Cje Down syndrome model mice or C57Bl6/J mice. Trib1 expression in hematopoietic cells of Ts1Cje mice accelerated the onset of AML development compared with that in wild type mice. Gene expression analysis showed up-regulation of Hox downstream genes and down-regulation of genes for the myeloid differentiation program and C/EBP targets. These results suggest that Trib1-mediated signaling plays an important role in promoting leukemogenesis in Down syndrome. We used microarrays to detail the global program of gene expression in mouse AML
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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. A 48 array study with 24 arrays for placenta and 24 for fetal liver. For each tissue we used RNA from 24 individual embryos, i.e. six male and six female embryos from both genotypes.
2011-05-11 | E-GEOD-24272 | biostudies-arrayexpress
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.
2010-07-16 | GSE17760 | GEO