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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

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

PROVIDER: PRJNA1000985 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25487142_1.fastq.gz	Fastqsanger.gz
	SRR25487142_2.fastq.gz	Fastqsanger.gz
	SRR25487143_1.fastq.gz	Fastqsanger.gz
	SRR25487143_2.fastq.gz	Fastqsanger.gz
	SRR25487144_1.fastq.gz	Fastqsanger.gz

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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

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

Project description:We performed bulk RNAseq on whole hearts from E13.5 Dp1Tyb embryos and from wild-type littermates, as well as hearts from E13.5 Dp1TybDyrk1a+/+/- embryos and wild-type littermates. Analysis showed the expected increased expression of the Hsa21-orthologous genes on Mmu16 that are present in 3 copies. Gene set enrichment analysis identified pathways that are altered in Dp1Tyb hearts. Some of these changes were dependent on 3 copies of Dyrk1a.

2024-01-25 | GSE196445 | GEO

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

Project description:We performed single cell RNAseq on whole hearts from E13.5 Dp1Tyb embryos and from wild-type littermates, as well as hearts from E13.5 Dp1TybDyrk1a+/+/- embryos and wild-type littermates. We identified 14 clusters which were assigned to individual cell types based on expression of marker genes.

2024-01-25 | GSE196446 | GEO

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

| PRJNA804913 | ENA

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

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

| PRJNA804912 | ENA

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

Project description:Down Syndrome (DS) results from the trisomy of human chromosome 21 (HSA21). It is still the most frequent intellectual disability, affecting 1 newborn per 700 births. Among candidate genes explaining intellectual disabilities seen in DS patients, the dual specificity tyrosine-phosphorylation regulated kinase 1A, DYRK1A, is located in the DS critical region of chromosome 21. DYRK1A has become a major screening target for the development of selective and potent pharmacological inhibitors. We here investigated the effects of a relatively selective DYRK1A inhibitor, Leucettine 41 (hereafter L41) in three different trisomic mouse models with increasing genetic complexity, Tg(Dyrk1a), Ts65Dn and Dp1Yey. Leucettines are derived from the marine sponge alkaloid Leucettamine B.

2018-10-17 | PXD008419 | Pride

Effects of Dyrk1a and Kcnj6 normalization on the hippocampal transcriptome in the Dp(16)1/Yey mouse model of Down syndrome

Project description:Down syndrome (DS), the most common human chromosomal disorder, is caused by trisomy 21. Recent studies show that the trisomic genes Dyrk1a and Kcnj6 play critical causative roles in DS cognitive deficits. Interestingly, an unexpected lack of improvement of hippocampal-dependent learning and memory deficits was observed when both Dyrk1a and Kcnj6 were normalized to diploidy in the DS mouse model, Dp(16)1/Yey (Dp16). In this study, we explored the molecular mechanisms underlying this phenomenon by using whole genome-wide hippocampal transcriptome analysis. In total, 142, 142, and 112 genes were found significantly differentially expressed in the Dp16, Dp16/Dyrk1aKO (Dyrk1a normalized) and Dp16;Dyrk1aKO/Kcnj6KO (Both Dyrk1a and Kcnj6 normalized) hippocampus, respectively, compared with the WT hippocampus. The majority of the common significantly differentially expressed genes (DEGs) were trisomic genes. Dyrk1a and Kcnj6 normalization mainly altered the expression of diploid genes. Normalizing Dyrk1a in the Dp16 hippocampus caused an overall downregulation of genes, whereas further Kcnj6 normalization caused an overall upregulation of genes. Both further rescuing effects and neutralizing effects were observed in Kcnj6 and Dyrk1a double-normalized mice compared with mice with Dyrk1a normalization alone.

2020-10-01 | GSE138468 | GEO

Expression data in the cerebral cortex of postnatal Dyrk1a+/+ and Dyrk1a+/- mice

Project description:DYRK1A is a protein kinase with several roles in brain development. This kinase is involved in two intellectual disability syndromes: Down syndrome and DYRK1A haploinsufficiency syndrome. The Dyrk1a+/- mouse is a model for DYRK1A haploinsufficiency syndrome. We used microarray to evaluate the impact of DYRK1A haploinsufficiency in the development of the cerebral cortex.

2019-03-06 | GSE127707 | GEO

Transcriptomic analysis of human foetal hearts with or without Down Syndrome

Project description:We performed bulk RNAseq on whole hearts from foetuses with Down syndrome and age-matched, sex-matched euploid controls. Analysis showed the expected increased expression of the genes on Hsa21 that are present in 3 copies. Gene set enrichment analysis identified pathways that are altered in DS hearts.

2024-01-25 | GSE196443 | GEO

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