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Transcriptome profiling of NUP133 mutant podocytes

ABSTRACT: Transcriptome profiling of NUP133 mutant podocytes

PROVIDER: PRJNA784261 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17055242_1.fastq.gz	Fastqsanger.gz
	SRR17055242_2.fastq.gz	Fastqsanger.gz
	SRR17055243_1.fastq.gz	Fastqsanger.gz
	SRR17055243_2.fastq.gz	Fastqsanger.gz
	SRR17055244_1.fastq.gz	Fastqsanger.gz

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Transcriptome profiling of NUP133 mutant podocytes

Project description:We generated NUP133 mutant podocytes to model human hereditary SRNS in vitro. A subtype of SRNS is caused by monogenetic mutations of the nuclear pore complex including NUP133. Human immortalized podocytes were genome edited applying the CRISPR/Cas9 technique to create NUP133 KO cells (“KO-1”). cDNA of NUP133-WT or causative variants NUP133 c.2922T>G (“Mutation-1”) or NUP133 c.3335-11T>A (“Mutation-2”) were stable expressed into this KO background by lentiviral transduction. Transcriptome profiling (RNA-Sequencing) and differential gene expression analysis was performed in triplicate for each cell line. NUP133 mutant podocytes showed no overt transcriptional changes compared to NUP133-WT cells.

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Transcriptome profiling of NUP133 WT and KO podocytes

Project description:We generated NUP133 WT and KO podocytes to model human hereditary SRNS in vitro. A subtype of SRNS is caused by monogenetic mutations of the nuclear pore complex including NUP133. Immortalized human podocytes were genome edited applying the CRISPR/Cas9 technique and two independent NUP133 sgRNAs. Two monoclonal cell backgrounds were used to create two matching sets of NUP133 WT and KO cells (WT-1 versus KO-1 and WT-2 versus KO-2). Transcriptome profiling (RNA-Sequencing) and differential gene expression analysis was performed in duplicate for each cell line. NUP133 KO podocytes exhibit vast transcriptional changes compared to WT cells.

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Transcriptome profiling of NUP133 WT and KO podocytes

Project description:Transcriptome profiling of NUP133 WT and KO podocytes

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Project description:To study the function of zebrafish nuclear pores during early embryogenesis, we generated maternal zygotic double mutant of nup85;nup133 (MZnup85;nup133) using CRISPR/Cas9 and report the transcriptome-wide changes in comparison to wild-type (WT) embryos. Our analysis reveals a dramatic delay of maternal mRNA degradation and zygotic genome activation in MZnup85;nup133 embryos during maternal-to-zygotic transition.

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Transcriptome profiling of EPB41L5 WT and KO podocytes

Project description:We generated EPB41L5 WT and KO podocytes to model human glomerular kidney disease in vitro. Immortalized human podocytes were genome edited applying the CRISPR/Cas9 technique. Two monoclonal cell lines were generated for WT and KO genotypes (WT-1, WT-2, KO-1 & KO-2). Transcriptome profiling (RNA-Sequencing) and differential gene expression analysis was performed in duplicate for each cell line. EPB41L5 KO podocytes exhibit transcriptional changes compared to WT cells. Analyzed cell were previously described: Schell C, Rogg M, Suhm M, et al. The FERM protein EPB41L5 regulates actomyosin contractility and focal adhesion formation to maintain the kidney filtration barrier. Proc Natl Acad Sci U S A. 2017;114(23):E4621-E4630. doi:10.1073/pnas.1617004114

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Project description:To investigate the function of nuclear pore complex (NPC) in the regulation of zygotic genome activation (ZGA), we established mutants of nucleoporins, including maternal and zygotic mutant of nup133 (MZnup133) and maternal mutant of elys (Melys), for maternal depletion by CRISPR/Cas9, and transgenic embryos of nup133 (Tgnup133) for maternal overexpression through Tol2 mediated method. We then performed gene expression profiling analysis using data obtained from RNA-seq of wildtype, MZnup133, Melys and Tgnup133 at three time points.

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Project description:Transcriptome profiling of EGFP and TEADi expressing podocytes

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Transcriptome profiling of EPB41L5 WT and KO podocytes

Project description:Transcriptome profiling of EPB41L5 WT and KO podocytes

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Transcriptome profiling of EGFP and TEADi expressing podocytes

Project description:EGFP (control) and TEADi expressing podocytes were generated by lentivirus transduction to analyze transcriptional signaling by YAP/TAZ-TEAD. Tetracycline-inducible TEADi is a GFP-tagged inhibitor of the interaction of YAP1 and TAZ with TEAD transcription factors. pInducer20 EGFP-TEADi was a gift from Ramiro Iglesias-Bartolome (Addgene plasmid # 140145 ; http://n2t.net/addgene:140145 ; RRID:Addgene_140145). TEADi was previously described: YAP1/TAZ-TEAD transcriptional networks maintain skin homeostasis by regulating cell proliferation and limiting KLF4 activity. Yuan Y., Park J., Feng A., Awasthi P., Wang Z., Chen Q., Iglesias-Bartolome R.. Nat Commun 11, 1472 (2020). 10.1038/s41467-020-15301-0. Transcriptome profiling (RNA-Sequencing) and differential gene expression analysis of 3 independent replicates per genotype was performed. TEADi podocytes exhibit transcriptional changes compared to WT cells including downregulation of prominent YAP target genes like CTGF, CYR61 and ANKRD1.

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NUP133 Controls Nuclear Pore Assembly, Transcriptome Composition, and Cytoskeleton Regulation in Podocytes.

Project description:Steroid-resistant nephrotic syndrome (SRNS) frequently leads to end-stage renal disease, ultimately requiring kidney replacement therapies. SRNS is often caused by hereditary monogenic mutations, specifically affecting specialized epithelial cells (podocytes) of the glomerular filtration barrier. Mutations in several components of the nuclear pore complex, including NUP133 and NUP107, have been recently identified to cause hereditary SRNS. However, underlying pathomechanisms, eliciting podocyte-specific manifestations of these nucleoporopathies, remained largely elusive. Here, we generated an in vitro model of NUP133-linked nucleoporopathies using CRISPR/Cas9-mediated genome editing in human podocytes. Transcriptome, nuclear pore assembly, and cytoskeleton regulation of NUP133 loss-of-function, mutant, and wild-type podocytes were analyzed. Loss of NUP133 translated into a disruption of the nuclear pore, alterations of the podocyte-specific transcriptome, and impaired cellular protrusion generation. Surprisingly, comparative analysis of the described SRNS-related NUP133 mutations revealed only mild defects. Am impaired protein interaction in the Y-complex and decrease of NUP133 protein levels might be the primary and unifying consequence of mutant variants, leading to a partial loss-of-function phenotype and disease manifestation in susceptible cell types, such as podocytes.

| S-EPMC9025798 | biostudies-literature

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