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Small RNA-sequencing of FUS H517Q and healthy iPSC-derived motor neurons

ABSTRACT: Small RNA-sequencing of FUS H517Q and healthy iPSC-derived motor neurons

PROVIDER: PRJNA838952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19241977.fastq.gz	Fastqsanger.gz
	SRR19241978.fastq.gz	Fastqsanger.gz
	SRR19241979.fastq.gz	Fastqsanger.gz
	SRR19241980.fastq.gz	Fastqsanger.gz
	SRR19241981.fastq.gz	Fastqsanger.gz

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FUS H517Q and healthy iPSC-derived motor neurons

Project description:FUS H517Q and healthy iPSC-derived motor neurons

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Small RNA-sequencing of FUS H517Q and healthy iPSC-derived motor neurons

Project description:We sought to investigate changes in expression levels of small RNAs including microRNAs in FUS H517Q and healthy motor neurons Motor neurons were differentiated from patient-derived FUS H517Q and healthy iPSCs, and harvested at day 30. We performed gene expression profiling analysis using data obtained from bulk small RNA-seq.

2022-05-20 | GSE203170 | GEO

Bulk RNA-sequencing of FUS H517Q and healthy iPSC-derived motor neurons

Project description:We sought to investigate changes in gene expression levels including changes in pri-microRNAs in FUS H517Q motor neurons Motor neurons were differentiated from patient-derived FUS H517Q and healthy iPSCs, and harvested at day 30. We performed gene expression profiling analysis using data obtained from bulk RNA-seq.

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Bulk RNA-sequencing of FUS H517Q and healthy iPSC-derived motor neurons

Project description:Bulk RNA-sequencing of FUS H517Q and healthy iPSC-derived motor neurons

| PRJNA838953 | ENA

Integrated profiling of iPSC-derived motor neurons carrying C9orf72, FUS, TARDBP, or SOD1 mutations

Project description:We conducted temporal RNA-seq profiling of human induced pluripotent stem cells (hiPSCs) and iPSC-derived motor neurons (iMNs) carrying C9orf72, FUS, TARDBP, or SOD1 mutations in both patients with ALS and healthy individuals. We discovered dysregulated gene expression and alternative splicing (AS) throughout iMN development and maturation, and iMNs with mutations in ALS-associated genes displayed enrichment of cytoskeletal defects and synaptic alterations from the premature stage to mature iMNs. Our findings indicate that synaptic gene dysfunction is a common molecular hallmark of familial ALS, which may result in neuronal susceptibility and progressive motor neuron degeneration. Analysis of upstream splicing factors revealed that differentially expressed RNA-binding proteins (RBPs) in iMNs from patients with ALS may cause abnormal AS events, highlighting the importance of studying RBP defects in ALS research. Overall, our research provides a comprehensive and valuable resource for gaining insights into the shared mechanisms of familial ALS pathogenesis during motor neuron development and maturation in iMN models.

2025-06-24 | GSE299997 | GEO

HTA2.0 (human transcriptome array) analysis of control iPSC-derived motor neurons (MN), FUS-H517D-hetero-iPSC-MN, and FUS-H517D-homo-iPSC-MNs

Project description:To assess RNA regulation in the MN possessing mutated FUS-H517D gene. Fused in sarcoma/translated in liposarcoma (FUS) is a causative gene of familial amyotrophic lateral sclerosis (fALS). Mutated FUS causes accumulation of DNA damage stress and stress granule (SG) formation, etc., thereby motor neuron (MN) death. However, key molecular etiology of mutated FUS-dependent fALS (fALS-FUS) remains unclear. Here, Bayesian gene regulatory networks (GRN) calculated by Super-Computer with transcriptome data sets of induced pluripotent stem cell (iPSC)-derived MNs possessing mutated FUSH517D (FUSH517D MNs) and FUSWT identified TIMELESS, PRKDC and miR-125b-5p as "hub genes" which influence fALS-FUS GRNs. miR-125b-5p expression up-regulated in FUSH517D MNs, showed opposite correlations against FUS and TIMELESS mRNA levels as well as reported targets of miR-125b-5p. In addition, ectopic introduction of miR-125b-5p could suppress mRNA expression levels of FUS and TIMELESS in the cells. Furthermore, we found TIMELESS and PRKDC among key players of DNA damage stress response (DDR) were down-regulated in FUSH517D MNs and cellular model analysis validated DDR under impaired DNA-PK activity promoted cytosolic FUS mis-localization to SGs. Our GRNs based on iPSC models would reflect fALS-FUS molecular etiology.

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Gene expression from human iPSC derived motor neurons.

Project description:Gene expression from human iPSC derived motor neurons.

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Expression profiles of primary motor neurons after knocking down Fus

Project description:To clarify the functional properties of FUS, we established the differentially expressed alternative exons in FUS-silenced primary motor neurons by using exon-sensitive microarray technology. To clarify the functional properties of FUS, we established the differentially expressed alternative exons in FUS-silenced primary glial cells by using exon-sensitive microarray technology. To clarify the functional properties of FUS, we established the differentially expressed alternative exons in FUS-silenced primary cerebellar neurons by using exon-sensitive microarray technology.

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Changes in FUS interactome in motor neurons upon ALS-related mutation

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