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Trisomy 21 and RNA-seq of family

ABSTRACT: Trisomy 21 and RNA-seq of family

PROVIDER: PRJNA962948 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24348234_1.fastq.gz	Fastqsanger.gz
	SRR24348234_2.fastq.gz	Fastqsanger.gz
	SRR24348235_1.fastq.gz	Fastqsanger.gz
	SRR24348235_2.fastq.gz	Fastqsanger.gz
	SRR24348236_1.fastq.gz	Fastqsanger.gz

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Trisomy 21 and RNA-seq of family

Project description:RNA-seq of lymphoblastoid cells from a family of individuals (one of which has Trisomy 21) was used to determine the molecular origin of dosage compensation in Trisomy 21.

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Trisomy 21 and GRO-seq of family

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Trisomy 21 and GRO-seq of family

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Project description:Gene expression was measured in trisomy 21 and trisomy 13 human fetal samples. For TS21, regions assayed were cerebrum, cerebellum, heart, and cerebrum-derived astrocyte cell lines. Keywords = trisomy 21 Keywords = Down syndrome Keywords = aneuploidy Keywords = brain Keywords = heart Keywords = trisomy 13 Keywords: other

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RNA-seq of human aneuploid cell lines with Trisomy 21

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Project description:Down syndrome, caused by trisomy 21, is a complex developmental disorder associated with intellectual disability and reduced growth of multiple organs. Structural pathologies are present at birth, reflecting embryonic origins. A fundamental unanswered question is how an extra copy of human chromosome 21 contributes to organ-specific pathologies that characterize individuals with Down syndrome. Relevant to the hallmark intellectual disability in Down syndrome, how does trisomy 21 affect neural development? We tested the hypothesis that trisomy 21 exerts effects on human neural development as early as neural induction. Bulk RNA sequencing was performed on isogenic trisomy 21 and euploid human induced pluripotent stem cells (iPSCs) at successive stages of neural induction: embryoid bodies at Day 6, early neuroectoderm at Day 10, and differentiated neuroectoderm at Day 17. Gene expression analysis revealed over 1,300 differentially expressed genes in trisomy 21 cells along the differentiation pathway compared to euploid controls. Less than 5% of the gene expression changes included upregulated chromosome 21 encoded genes at every timepoint. Genes involved in specific growth factor signaling pathways (Wnt and Notch), metabolism (including interferon response and oxidative stress), and extracellular matrix were altered in trisomy 21 cells. Further analysis revealed heterochronic expression of genes. This comprehensive analysis reveals that trisomy 21 impacts discrete developmental pathways at the earliest stages of neural development. Further, the results suggest that metabolic dysfunction arises early in embryogenesis in trisomy 21 and may thus affect development and function more broadly.

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Myocardial Reprogramming by HMGN1 Underlies Heart Defects in Trisomy 21 [scRNA-seq]

Project description:Congenital heart defects (CHD) are the most common form of developmental abnormalities, occurring in ~1% of live births, and can arise due to altered dosage of genes essential for cardiogenesis. Aneuploidy accounts for nearly 15% of CHD and the most frequent form involves trisomy of chromosome 21 (Ch21), resulting in Down Syndrome (DS). Here we used single cell RNA-seq, CRISPR-activation with single cell RNA-seq, single cell ATAC-seq and Cut&Tag epigenomic profiling to define the molecular disruptions occuring with Trisomy 21 and upregulation of the Ch21 epigenetic factor HMGN1. These experiments were performed in human pluripotent stem cells (hiPSCs) or in directed differentiation to cardiomyocyte lineages at days 10 and 20.

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Transcriptome analysis by RNA sequencing of human trisomy 21 and normal control blood cells

Project description:The aim of this study is to analyse trisomy 21 (T21) transcriptome. We generated RNA sequencing (RNA-Seq) paired-end data from ribosomal RNA-depleted total RNA isolated from blood cell samples of four T21 and four normal control individuals.

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Gene expression variation increase in trisomy 21 tissues

Project description:Congenital development disorders with variable severity occur in trisomy 21. However, how these phenotypic abnormalities develop with variations remains elusive. We hypothesize that the difference in euploidy gene expression variation among trisomy 21 tissues are perturbed by the presence of an extra copy of chromosome 21 and this may contribute to the phenotypic variations in Down syndrome. Keywords: Disease state analysis

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