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Large-scale study suggests effects of trisomy 21 on fetal neurodevelopment may be more subtle than variability between organoids and isogenic lines

ABSTRACT: Large-scale study suggests effects of trisomy 21 on fetal neurodevelopment may be more subtle than variability between organoids and isogenic lines

PROVIDER: PRJNA920518 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23008400_1.fastq.gz	Fastqsanger.gz
	SRR23008400_2.fastq.gz	Fastqsanger.gz
	SRR23008401_1.fastq.gz	Fastqsanger.gz
	SRR23008401_2.fastq.gz	Fastqsanger.gz
	SRR23008402_1.fastq.gz	Fastqsanger.gz

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Large-scale study suggests effects of trisomy 21 on fetal neurodevelopment may be more subtle than variability between organoids and isogenic lines

Project description:This study examines cortical organoids generated from a panel of isogenic trisomic and disomic iPSC lines (subclones) as a model of early fetal brain development in Down syndrome. An initial experiment comparing organoids from one trisomic and one disomic line showed many genome-wide transcriptomic differences and modest differences in cell-type proportions, suggesting there may be a neurodevelopmental phenotype that is due to trisomy of chr 21. To better control for multiple sources of variation, we undertook a highly robust study of ∼1,200 organoids using an expanded panel of six all-isogenic lines, three disomic, and three trisomic. The power of this experimental design was indicated by strong detection of the ∼1.5- fold difference in chr21 genes. However, the numerous expression differences in non-chr21 genes seen in the smaller experiment fell away, and the differences in cell-type representation between lines did not correlate with trisomy 21. Results suggest that the initial smaller experiment picked up differences between small organoid samples and individual isogenic lines, which “averaged out” in the larger panel of isogenic lines. Our results indicate that even when organoid and batch variability are better controlled for, variation between isogenic cell lines (even subclones) may obscure, or be conflated with, subtle neurodevelopmental phenotypes that may be present in ∼2nd trimester DS brain development. Interestingly, despite this variability between organoid batches and lines, and the “fetal stage” of these organoids, an increase in secreted Aβ40 peptide levels—an Alzheimer-related cellular phenotype—was more strongly associated with trisomy 21 status than were neurodevelopmental shifts in cell-type composition.

2023-01-07 | GSE222365 | GEO

Large-scale organoid study suggests effects of trisomy 21 on early fetal neurodevelopment are more subtle than variability between isogenic lines and experiments.

Project description: Not available

| S-EPMC9935940 | biostudies-literature

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

2005-05-10 | GSE1397 | GEO

The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome

Project description:Down syndrome (DS) is caused by trisomy for human chromosome 21 (Hsa21) and is associated with atypical neurodevelopment that begins prenatally. The developing human fetus receives nutritional support and gas exchange from the placenta, and normal placental function is essential for proper development. Placentas that sustain fetuses with trisomy 21 contain trisomic cells, but little is known about which trisomic genes are overexpressed in the placenta or their downstream molecular, cellular, and functional effects. Mouse models of DS are useful in vivo systems for studying the prenatal effects of trisomy. This study examined the placental transcriptome in four mouse models of DS: Dp(16)1/Yey, Ts65Dn, Ts66Yah, and Ts1Cje. Despite modest overlap of trisomy-associated gene dysregulation among these four models, pathway enrichment analyses identified alterations in extracellular matrix pathways in all four models and notable upregulation of immune system pathways in Dp(16)1/Yey and Ts66Yah.

2025-12-08 | GSE303248 | GEO

5-hydroxymethylcytosine-mediated epigenetic dynamics during neurodevelopment and aging

Project description:This SuperSeries is composed of the following subset Series: GSE32050: 5-hydroxymethylcytosine-mediated epigenetic dynamics during neurodevelopment and aging [5hmC Capture and Seq] GSE32187: 5-hydroxymethylcytosine-mediated epigenetic dynamics during neurodevelopment and aging [mRNA profiling] Refer to individual Series

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Trisomy-TAC-seq

Project description:Trisomy-TAC-seq

| PRJNA431465 | ENA

Trisomy-TAC-seq II

Project description:Trisomy-TAC-seq II

| PRJNA498711 | ENA

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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Trisomy detection by PCR and comparative genomic hybridization

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