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RNA-seq of human K562 leukemia cells with or without a mutation in SF3B1 (splicing factor 3b, subunit 1) that were treated with DMSO or the STAT3 inhibitor STATTIC

ABSTRACT: The purpose of the experiment was to define the gene expression and splicing alterations occurring when human wildtype or splicing factor 3b subunit 1 (SF3B1) mutant K562 cells had STAT3 inhibited with the small molecule STATTIC. Results provide insight the interplay of SF3B1 and STAT3 in human hematopoietic cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206020 | GEO | 2022/12/13

REPOSITORIES: GEO

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RNA-seq of endothelial cells from 28 hours post fertilization sf3b1 mutant and sibling zebrafish with Stat3 overexpression

Project description:The purpose of the experiment was to define the gene expression and splicing alterations occurring when wildtype or consitutively active Stat3 are expressed in embryonic zebrafish endothelial cells with low levels of splicing factor 3b subunit 1 (Sf3b1). Results provide insight the interplay of Sf3b1 and Stat3 in hematopoietic development.

2022-12-13 | GSE206019 | GEO

Transcriptome analysis of SF3B1-mutation induced changes in K562 cells

Project description:Using RNA-Seq, we determined changes to gene expression and splicing on inducible expression of SF3B1-WT and SF3B1-MUT (K700E) in K562 cells. Using RNA-Seq, we determined changes to gene expression and splicing on inducible expression of SF3B1-WT and SF3B1-MUT (K700E) in K562 cells.

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Differential gene expression and exon usage in bone marrow from RARS patients with SF3B1 somatic mutations compared to healthy patients.

Project description:SF3B1, splicing factor 3b subunit 1 is a component of the RNA splicing machinery and it has been found to be highly mutated in refractory anemia with ring sideroblasts (RARS) and RARS associated with thrombocytosis (RARS-T). The aim of this study is to investigate the RNA splicing patterns in bone marrow from patients with SF3B1 somatic mutations compared to normal physiologic splicing. We compared the RNA splicing pattern as exon usage, differential gene expression, and pathway analysis with normal splicing mRNA profiles, as measured by RNA-Seq, in bone marrow derived mononuclear cells from 2 RARS patients with SF3B1 somatic mutations were compared to the mRNA profile of a normal donor.

2013-01-18 | E-GEOD-43603 | biostudies-arrayexpress

RNA-seq of endothelial cells from 28 hours post fertilization sf3b1 mutant and sibling zebrafish

Project description:The purpose of the experiment was to define the gene expression and splicing alterations occurring when the levels of splicing factor 3b subunit 1 (Sf3b1) are lowered in embryonic zebrafish. Results provide insight the role of Sf3b1 in hematopoietic development.

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RNA sequencing of bone marrow CD34+ cells from myelodysplastic syndrome patients with and without SF3B1 mutation and from healthy controls

Project description:The splicing factor SF3B1 is the most commonly mutated gene in the myelodysplastic syndromes (MDS), particularly in patients with refractory anemia with ring sideroblasts (RARS). MDS is a disorder of the hematopoietic stem cell and we thus studied the transcriptome of CD34+ cells from MDS patients with SF3B1 mutations using RNA-sequencing. Genes significantly differentially expressed at the transcript and/or exon level in SF3B1 mutant compared to wildtype cases include genes involved in MDS pathogenesis (ASXL1, CBL), iron homeostasis and mitochondrial metabolism (ALAS2, ABCB7, SLC25A37) and RNA splicing/processing (PRPF8, HNRNPD). Many genes regulated by a DNA damage-induced BRCA1-BCLAF1-SF3B1 protein complex showed differential expression/splicing in SF3B1 mutant cases. Our data indicate that SF3B1 plays a critical role in MDS by affecting the expression and splicing of genes involved in specific cellular processes/pathways, many of which are relevant to the known RARS pathophysiology, suggesting a causal link. RNA-Seq was performed to compare the transcriptome of bone marrow CD34+ cells from eight MDS patients with SF3B1 mutation, four MDS patients with no known splicing mutation and five healthy controls.

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SF3B1 association with chromatin determines splicing outcomes

Project description:Much remains unknown concerning the mechanism by which the splicing machinery pinpoints short exons within intronic sequences and how splicing factors are directed to their pre-mRNA targets. Part of the explanation probably lies in differences in chromatin organization between exons and introns. Proteomic, co-immunoprecipitation, and sedimentation analyses described here indicated that SF3B1, an essential splicing component of the U2 snRNP complex, is strongly associated with nucleosomes. ChIP-seq and RNA-seq analyses revealed that SF3B1 is specifically bound to nucleosomes located at exonic positions. SF3B1 binding is enriched at nucleosomes positioned over short exons flanked by long introns that are also characterized by differential GC content between exons and introns. Disruption of SF3B1 binding to such nucleosomes affected the splicing of these exons similarly to inhibition of SF3B1 expression. Our findings suggest that the association of SF3B1 with nucleosomes is functionally important for splice site recognition and that SF3B1 conveys splicing-relevant information embedded in chromatin structure. MNase-seq on Input and SF3B1 pull-down, mRNA-seq on control and SF3B1 si-RNA treated cells as well as on TSA (Trichostatin A) treated and untreated cells.

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SF3B1 Degron knockdown RNA-seq

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Differential gene expression and exon usage in bone marrow from RARS patients with SF3B1 somatic mutations compared to healthy patients.

2013-01-18 | GSE43603 | GEO

SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [ChIP-Seq]

Project description:Splicing factor 3b subunit 1 (SF3B1) is one of the most frequently mutated spliceosomal components in cancer. Recent studies additionally imply an involvement of the wildtype protein in tumor progression, but the underlaying mechanism remains elusive. Here we report that SF3B1 acts as a coactivator for hypoxia-inducible factor (HIF) 1α. SF3B1 directly interacts with HIF1a, augments HIF1a-HIF1b heterodimer binding to hypoxia response elements in vivo and enhances transactivation of HIF target genes. In human patients, primary patient cells and in a mouse model of pancreatic ductal adenocarcinoma (PDAC), efficient HIF1a-signalling relies on SF3B1. Monoallelic deletion of Sf3b1 in this mouse tumor model severely delays tumor initiation and development and diminishes HIF target gene transcription, glucose uptake and proliferation in corresponding tumor organoids in hypoxia, while splicing remains functional. Here, we define a subset of aggressive chromophobe renal cell carcinomas (chRCCs) able to transcriptionally compensate monoallelic SF3B1 loss, a feature that correlates with poor prognosis and lymph node spread and we show that the oncogenic hotspot mutation SF3B1K700E has reduced co-activation efficiency. Also, we report increased sensitivity of cells with low levels of SF3B1 to the HIF-inhibitor PX-478. These findings reveal a splicing-independent, tumor promoting function of SF3B1, important in the pathogenesis of PDAC and other cancers.

2022-06-22 | GSE201461 | GEO

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