Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression + ATAC profiling of trisomic hippocampal neurons upon SAHA treatment [ATAC-seq]

ABSTRACT: Down syndrome (DS) is associated with widespread molecular alterations, including aberrant gene expression, which not only affects chromosome 21 genes but perturbs the whole transcriptome. The genome-wide nature of this alteration suggests that it might be epigenetically mediated, which may also offer therapeutic opportunities given the reversibility of epigenetic modifications. Here, we show that decreased global acetylation level in the hippocampus of the trisomic mouse model Ts65Dn is associated with decreased chromatin accessibility at gene promoters in hippocampal neurons. Strikingly, pharmacological restoration of histone acetylation using the clinically approved histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) normalized transcriptomic, epigenetic and cortico-hippocampal memory deficits in trisomic mice. This rescue was mediated by an unexpected heterochromatization of the supernumerary chromosome. Altogether, our results identify an unanticipated epigenetic mechanism linking histone acetylation dynamics to chromosomal dosage homeostasis.

ORGANISM(S): Mus musculus

PROVIDER: GSE328495 | GEO | 2026/08/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression + ATAC profiling of trisomic hippocampal neurons upon SAHA treatment [RNA-seq]

Project description:Down syndrome (DS) is associated with widespread molecular alterations, including aberrant gene expression, which not only affects chromosome 21 genes but perturbs the whole transcriptome. The genome-wide nature of this alteration suggests that it might be epigenetically mediated, which may also offer therapeutic opportunities given the reversibility of epigenetic modifications. Here, we show that decreased global acetylation level in the hippocampus of the trisomic mouse model Ts65Dn is associated with decreased chromatin accessibility at gene promoters in hippocampal neurons. Strikingly, pharmacological restoration of histone acetylation using the clinically approved histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) normalized transcriptomic, epigenetic and cortico-hippocampal memory deficits in trisomic mice. This rescue was mediated by an unexpected heterochromatization of the supernumerary chromosome. Altogether, our results identify an unanticipated epigenetic mechanism linking histone acetylation dynamics to chromosomal dosage homeostasis.

2026-08-07 | GSE328496 | GEO

Gene expression + ATAC profiling of trisomic hippocampal neurons upon SAHA treatment [ATAC-seq]

Project description:Gene expression + ATAC profiling of trisomic hippocampal neurons upon SAHA treatment [ATAC-seq]

| PRJNA1455549 | ENA

Gene expression + ATAC profiling of trisomic hippocampal neurons upon SAHA treatment [RNA-seq]

Project description:Gene expression + ATAC profiling of trisomic hippocampal neurons upon SAHA treatment [RNA-seq]

| PRJNA1455548 | ENA

Mandibular precursor at E13.5 in Ts65Dn Down syndrome mouse

Project description:Gene expression of mandibular precursor from embryonic day 13.5 trisomic and euploid embryos from the Ts65Dn Down syndrome mouse model. Results provide insight into importance of non-trisomic genes in organogenesis.

2010-11-02 | GSE24554 | GEO

Molecular Cartography of the Human and Mouse Down Syndrome Brain [MERFISH]

Project description:Given the importance of linking human and model system pathobiology, we also performed highly multiplexed RNA in situ spatial transcriptomics on a well-established trisomic mouse model (Ts65Dn) to study the cellular landscape of the trisomic brain during early life and aging. We profiled the spatial transcriptome of > 240,000 cells in the mouse brain and identified trisomy-associated gene expression patterns in the molecular control of neurogenesis, gliogenesis, and myelination. Multiplexed error-robust fluorescence in situ hybridization (MERFISH) was performed on postnatal day 0 (P0) and 6 month (6mo) euploid and trisomic (Ts65Dn) mice (n=3 per condition). Coronal sections of the entire brain were used for analysis.

2025-07-11 | GSE280177 | GEO

Mandibular precursor at E13.5 in Ts65Dn Down syndrome mouse

2010-11-02 | E-GEOD-24554 | biostudies-arrayexpress

Affymetrix expression arrays from heart extracted RNA in Ts65Dn and Ms5Yah and Ts65DnMs5Yah mouse models

Project description:Affymetrix Mouse Gene 1.0 ST hydridization using wt extracts from adult mice hearts as controls and Ts65Dn, Ms5Yah and Ts65Dn/Ms5Yah samples. <br><br>N = 5 mices per group of genotype.<br><br>Goal : assess the gene dosage effect on partial trisomic/monosomic mice modelling human Down syndrome.

2011-10-05 | E-MEXP-3355 | biostudies-arrayexpress

The impact of Mmu17 non-Hsa21 orthologous genes in the Ts65Dn mouse model of Down syndrome: the “gold standard” refuted

Project description:Background: Despite successful preclinical treatment studies to improve neurocognition in the Ts65Dn mouse model of Down syndrome (DS), translation to humans has failed. This raises questions about the appropriateness of the Ts65Dn mouse as the “gold standard” for DS research. Here we used the novel Ts66Yah mouse that carries both an extra chromosome and the identical segmental Mmu16 trisomy as Ts65Dn without the Mmu17 non-orthologous region. Methods: Forebrains from embryonic day 18.5 Ts66Yah and Ts65Dn mice, along with euploid littermate controls, were used for gene expression and pathway analyses. Behavioral experiments were performed in neonatal and adult mice. Since male Ts66Yah mice are fertile, parent of origin transmission of the extra chromosome was studied. Results: We mapped 45 protein coding genes to the Ts65Dn Mmu17 non-orthologous, among which 71-82 % are expressed during forebrain development. Several of these genes were uniquely overexpressed in Ts65Dn embryonic forebrain; this produced major differences in dysregulated genes and pathways. Despite these genome-wide differences, the primary Mmu16 trisomic effects were highly conserved in both models, resulting in several commonly dysregulated disomic genes and pathways. Delays in motor development, communication and olfactory spatial memory were present in Ts66Yah but more pronounced in Ts65Dn neonates. Adult Ts66Yah mice showed working memory deficits and sex-specific effects in exploratory behavior and spatial hippocampal memory, while long-term memory was preserved. These deficits were milder when compared to Ts65Dn mice. Conclusions: Our findings suggest that triplication of the non-orthologous Mmu17 genes significantly contributes to the phenotype of the Ts65Dn mouse and may explain why preclinical trials that used this model have unsuccessfully translated to human therapies.

2023-01-16 | GSE222355 | GEO

RPE-1 and RPE-1 trisomic AHA p-c and steady state data

Project description:We developed a pulse-chase method in where fully SILAC (heavy, medium-heavy and Light) labelled cells were pulsed with Azidohomoalanine (AHA) and then chased for different length of times. In addition, steady state protein levels comparing the RPE- and RPE-1 trisomic cells by standard SILAC labeling was also acquired. These datasets contain data for the human RPE-1 and RPE-1 trisomic cell lines.

2016-10-06 | PXD004915 | Pride

Single Cell Analysis in trisomic tissues and organoids

Project description:Cortical organoids generated from mESC from a Down Syndrome (DS) mouse model (Ts65Dn) were dissociated for single cell sequencing to understand whether differential gene expression in DS brains affects cell diversity and how the molecular events that control the development of these diverse types of neocortical neurons are affected by the trisomy. These results were generated in parallel to a single cell experiment in forebrain fetal tissue from WT and Ts65Dn mice.

2023-03-15 | E-MTAB-12827 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data