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Trisomy 21 human iPSC derived interneuron progenitors

ABSTRACT: Trisomy 21 human iPSC derived interneuron progenitors

PROVIDER: PRJNA832126 | ENA |

REPOSITORIES: ENA

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Trisomy 21 human iPSC derived interneuron progenitors

Project description:Individuals with Down syndrome (DS, Ts21) have impaired neurogenesis during development. Using Ts21 human induced pluripotent stem cells (iPSCs) and isogenic controls, we carried out single cell RNA-sequencing of Ts21 interneuron progenitors .

2022-07-18 | GSE201523 | GEO

Transcriptome profiling of trisomy 21 and euploid iPSC-derived hematopoietic progenitors expressing wtGATA1 or an amino-truncated isoform of GATA1, GATA1short (GATA1s).

Project description:We generated human induced pluripotent stem cells (iPSCs) from trisomy 21 (T21) and euploid patient tissues with and without GATA1 mutations causing exclusive expression of truncated GATA1, termed GATA1short (GATA1s). Transcriptome analysis comparing expression levels of genes in GATA1s vs. wtGATA1-expressing progenitors demonstrated that GATA1s impairs erythropoiesis and enhances megakaryopoiesis and myelopoiesis in both T21 and euploid contexts in the iPSC-model system. We analyzed the transcriptome of (i) T21 iPSC-derived heamtopoietic progenitors expressing wtGATA1 (6 replicates) or GATA1s (3 replicates), as well as of (ii) euploid iPSC-derived progenitors expressing wtGATA1 (2 replicates) or GATA1s (2 replicates).

2015-01-26 | E-GEOD-36787 | biostudies-arrayexpress

Transcriptome profiling of trisomy 21 and euploid iPSC-derived hematopoietic progenitors expressing wtGATA1 or an amino-truncated isoform of GATA1, GATA1short (GATA1s).

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Expression data from trisomy 21 and euploid induced pluripotent stem cell hematopoietic progenitors

Project description:We modeled human Trisomy 21 primitive hematopoiesis using induced pluripotent stem cells (iPSCs). Primitive multipotent progenitor populations generated from Trisomy 21 iPSCs showed normal proliferative capacity and megakaryocyte production, enhanced erythropoiesis and reduced myeloid development compared to euploid iPSCs. CD41+/235+ iPSC-derived progenitor cells were flow cytometrically sorted for RNA extraction and hybridization onto Affymetrix microarrays.

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Trisomy 21 and TS13

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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Expression data from trisomy 21 and euploid induced pluripotent stem cell hematopoietic progenitors

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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.

2023-04-29 | GSE230995 | GEO

Trisomy 21 and GRO-seq of family

Project description:GRO-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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ATACseq : role of trisomy 21, GATAs mutation and associated mutations in the development of trisomy 21

Project description:Acute megakaryoblastic leukemia of Down syndrome (DS-AMKL) is a model of clonal evolution from a preleukemic transient myeloproliferative disorder requiring both a trisomy 21 (T21) and a GATA1s mutation to a leukemia driven by additional driver mutations. We modelled this leukemic evolution through stepwise gene editing of GATA1s, SMC3+/- and MPLW515K providing 20 different trisomy or disomy 21 iPSC clones. The CD41+/CD42+ MK were sorted (10 000 to 30 000 cells) and submitted to cell lysis, transposition, and purification steps. The transposed DNA fragments were amplified by PCR 12 times using adapters from the Nextera Index Kit (Illumina). PCR purification was performed using MinElute PCR Purification Kit (Qiagen, 28004) to remove large fragments and remaining primers. Library quality was assessed using an Agilent 2100 Bioanalyzer (Agilent Technologies 5067-4626). Libraries were sequenced using NovaSeq-6000 sequencer (Illumina; 50 bp paired-end reads).

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Transcriptional Consequences of Trisomy 21 on Neural Induction

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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