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The gene expression of primitive macrophage progenitors derived from Down syndrome model mouse embryonic stem cells on differentiation day 4

ABSTRACT: 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. We have shown that the number of microglia was decreased in the brain of Ts1Cje fetus, thereby we analyzed the effects of Ts1Cje trisomic region on differentiation of embryonic stem cells (ESCs) with genotype of Ts1Cje mice into primitive macrophage progenitors.

ORGANISM(S): Mus musculus

PROVIDER: GSE281248 | GEO | 2025/11/24

REPOSITORIES: GEO

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The gene expression of primitive macrophages derived from Down syndrome model mouse embryonic stem cells on differentiation day 12

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. We have shown that the number of microglia was decreased in the brain of Ts1Cje fetus, thereby we analyzed the effects of Ts1Cje trisomic region on differentiation of embryonic stem cells (ESCs) with genotype of Ts1Cje mice into primitive macrophages.

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

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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.

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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

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Project description:With an astounding incidence of ~1 in 800 births, Down syndrome (DS) is the most common chromosomal condition linked to intellectual disability worldwide. While the genetic basis of DS has been identified as a triplication of chromosome 21 (HSA21), the genes encoded from HSA21 that directly contribute to cognitive deficits remain incompletely understood. Here, we found that the HSA21-encoded chromatin effector, BRWD1, was upregulated in Down syndrome neurons and brain of trisomic mice. We showed that selective copy number restoration of Brwd1 in trisomic animals rescued deficits in hippocampal LTP, cognition and gene expression. We demonstrated that Brwd1 tightly binds the BAF chromatin remodeling complex, and that increased Brwd1 expression promotes BAF genomic mistargeting. Importantly, Brwd1 renormalization rescued aberrant BAF localization, along with associated changes in chromatin accessibility and gene expression. These findings establish BRWD1 as a key epigenomic mediator of normal neurodevelopment and an important contributor to DS-related phenotypes.

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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.

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Biomarkers for Down Syndrome screening in murine fetal liver and placenta

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Rescue of Down syndrome related deficits by Brwd1 copy number restoration

Project description:Trisomy 21 [Down syndrome/DS] is the most common genetic cause of intellectual disability worldwide. Despite much progress in the genetic characterization of DS, the genes encoded from chromosome 21 (HSA21) that directly contribute to intellectual disability remain incompletely understood. Here, we found that a largely uncharacterized chromatin effector protein, BRWD1, is triplicated in DS neurons and brain of trisomic mice. We demonstrated that selective copy number restoration of Brwd1 in DS animals rescues transcriptional, synaptic and cognitive deficits. We showed that Brwd1 binds to the neuronal BAF chromatin remodeling complex, and that such interactions promote BAF’s genomic mistargeting in DS-like brain. Brwd1 renormalization in trisomic animals rescues these aberrant chromatin events. These findings thus establish BRWD1 as a critical epigenomic mediator of DS related phenotypes.

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Correction of cognitive deficits in mouse models of Down syndrome by pharmacological inhibitor of DYRK1A

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