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Transcriptomic analysis of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using scRNAseq

ABSTRACT: We performed single cell RNAseq on whole hearts from E13.5 Dp1Tyb embryos and from wild-type littermates.

ORGANISM(S): Mus musculus

PROVIDER: GSE240137 | GEO | 2026/07/29

REPOSITORIES: GEO

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Effect of Dyrk1a inhibition on the transcriptome of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using bulk RNAseq

Project description:Embryos from the Dp1Tyb mouse model for Down syndrome (DS) present with congenital heart defects similar to the heart defects seen in humans with DS. We found that genetically reducing the copy number of the Dyrk1a gene (one of the genes in 3 copies in DS) from 3 to 2, normalised some of the transcriptomic changes in Dp1Tyb embryonic hearts and rescued congenital heart defects. Here we treated pregnant mice carrying Dp1Tyb and wild-type (WT) embryos with a Dyrk1a pharmacological inhibitor (Leucettinib-21 or L21) or an inactive isomer (Iso-L21) to study the effect of L21 on the transcriptome of Dp1Tyb and WT embryonic hearts.

2024-01-25 | GSE239798 | GEO

Transcriptomic analysis of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using scRNAseq

Project description:Transcriptomic analysis of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using scRNAseq

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Dyrk1a dosage effects on the transcriptome of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using scRNAseq

Project description:Dyrk1a dosage effects on the transcriptome of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using scRNAseq

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Does three copies of App contribute to amplified basal interferon signaling in the brain of the Dp1Tyb mouse model of Down syndrome

Project description:We have previously found that the Dp1Tyb mouse model of Down syndrome exhibits amplified basal interferon signaling in the brain but that the Dp2Tyb mouse does not unless challenged with interferon. The Dp1Tyb model carries an additional copy of the App gene, whereas the Dp2Tyb model does not. The additional copy of App has been suggested to contribute to altered neuroimmune biology in the brains of a genetically similar DS mouse model. Moreover, raised amyloid-β triggers interferon signaling in the brain of amyloid accumulation mouse models. Here we test if an additional copy of App contributes to altered interferon signaling in the Dp1Tyb mouse model of Down syndrome in the hippocampus.

2026-02-13 | GSE255679 | GEO

Transcriptome of Dp1Tyb and wild-type mouse embryonic fibroblasts

Project description:Purpose: to identify the effects of the Dp1Tyb mutation on the transcriptome of mouse embryonic fibroblasts

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Dyrk1a dosage effects on the transcriptome of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using bulk RNAseq

Project description:Dyrk1a dosage effects on the transcriptome of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using bulk RNAseq

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Effect of Dyrk1a inhibition on the transcriptome of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using bulk RNAseq

Project description:Effect of Dyrk1a inhibition on the transcriptome of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using bulk RNAseq

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Transcriptome of Dp1Tyb and wild-type mouse embryonic fibroblasts [ERCC spike-ins]

Project description:Purpose: to identify the effects of the Dp1Tyb mutation on the transcriptome of mouse embryonic fibroblasts

2019-03-29 | GSE123514 | GEO

Transcriptome of Dp1Tyb and wild-type mouse hippocampus

Project description:Purpose: to identify the effects of the Dp1Tyb mutation on the transcriptome of mouse hippocampus

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Discovery of DYRK1A dependent phosphorylation in mouse embryonic heart

Project description:The Dp1Tyb mouse model for Down syndrome contains a duplication of 23Mb of mouse chromosome 16 (Mmu16) that is orthologous to human chromosome 21 (Hsa21). This region contains 145 coding genes, and thus these genes are present in 3 copies. Dp1Tyb mice display congenital heart defects, similar to the ones seen in people with Down syndrome. These defects include ventricular and atrio-ventricular septal defects and are seen at embryonic day 14.5 (E14.5) of gestation. One of the 145 genes present in 3 copies in Dp1Tyb mice codes for a kinase called DYRK1A. We found that by crossing Dp1Tyb mice with mice carrying a heterozygous Dyrk1a loss of function allele, thereby reducing the dosage of the Dyrk1a gene from 3 to 2 copies, we rescue the congenital heart defects. Thus 3 copies of Dyrk1a are required to cause heart defects, and, presumably, increased DYRK1A protein is required for the heart defects. We compared the phosphoproteome in Dp1Tyb versus Dp1TybDyrk1a+/+/- embryonic hearts in order to discover alterations in phosphoproteins that could pinpoint molecular mechanisms that give rise to the congenital heart defects. The two strains (Dp1Tyb and Dp1TybDyrk1a+/+/-) differ only in the copy number of Dyrk1a (3 v 2) and thus differences in phosphoproteins would include both direct and indirect targets of DYRK1A activity.

2024-02-01 | PXD013053 | Pride

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