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RNA-seq of erythroid cells from 24 hours post fertilization sf3b1 mutant and sibling zebrafish

ABSTRACT: RNA-seq of erythroid cells from 24 hours post fertilization sf3b1 mutant and sibling zebrafish

PROVIDER: PRJNA533283 | ENA |

REPOSITORIES: ENA

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RNA-seq of erythroid cells from 24 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 the splicing factor Sf3b1 are lowered in embryonic zebrafish. Results provide insight the role of Sf3b1 in erythropoietic development.

2019-05-01 | GSE129952 | GEO

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.

2022-12-13 | GSE206017 | GEO

RNA-seq of erythroid cells from 40 hours post fertilization ddx41 mutant and sibling zebrafish

Project description:RNA-seq of erythroid cells from 40 hours post fertilization ddx41 mutant and sibling zebrafish

| PRJNA675042 | ENA

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

EIF2AK1-mediated signaling drives SF3B1 mutation-induced arrest in terminal erythroid differentiation in myelodysplastic syndrome with ringed sideroblasts

Project description:SF3B1 mutations, which occur in 20% of patients with myelodysplastic syndromes (MDS), are the hallmarks of a specific MDS subtype, MDS with ringed sideroblasts (MDS-RS), which is characterized by the accumulation of erythroid precursors in the bone marrow.

2022-07-30 | GSE188367 | GEO

SF3B1 mutant-induced missplicing of MAP3K7 causes anemia in myelodysplastic syndromes

Project description:SF3B1 is the most frequently mutated RNA splicing factor in cancer, including in ~25% of myelodysplastic syndromes (MDS) patients. SF3B1-mutated MDS, which is strongly associated with ringed sideroblast morphology, is characterized by ineffective erythropoiesis, leading to severe, often fatal, anemia. However, functional evidence linking SF3B1 mutations to the anemia described in MDS patients harboring this genetic aberration is weak, and the underlying mechanism is completely unknown. Using isogenic SF3B1 wild-type and mutant cell lines, normal human CD34 cells and MDS patient cells, we define a previously unrecognized role of the kinase MAP3K7, encoded by a known mutant SF3B1-targeted transcript, in controlling proper terminal erythroid differentiation, and show how MAP3K7 missplicing leads to the anemia characteristic of SF3B1-mutated MDS, although not to ringed sideroblast formation. We found that p38 MAPK is deactivated in SF3B1 mutant isogenic and patient cells and that MAP3K7 is an upstream positive effector of p38 MAPK. We demonstrate that disruption of this MAP3K7-p38 MAPK pathway leads to premature downregulation of GATA1, a master regulator of erythroid differentiation, and that this is sufficient to trigger accelerated differentiation, erythroid hyperplasia and ultimately apoptosis. Our findings thus define the mechanism leading to the severe anemia found in MDS patients harboring SF3B1 mutations.

2021-11-06 | GSE187356 | GEO

SF3B1 Degron knockdown RNA-seq

Project description:Knockdown of mutant and/or wild-type SF3B1 in MEL202 cell line by Degron knock-in, followed by RNA-seq, to identify splicing events governed by mutant SF3B1. Control: parental MEL202 cell line. Experiments: mutant-SF3B1 knockdown; wildtype-SF3B1 knockdown; mutant SF3B1 knockout. Treatments: each of these four conditions plus and minus shld.

2015-03-11 | E-GEOD-66719 | biostudies-arrayexpress

RNA-seq of erythroid cells from 40 hours post fertilization ddx41 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 dead-box helicase 41 are lowered in embryonic zebrafish. Results provide insight the role of Ddx41 in hematopoietic development.

2021-06-30 | GSE160979 | GEO

SF3B1 deficiency impairs human erythropoiesis via activation of p53 pathway: implications for understanding of ineffective erythropoiesis in MDS

Project description:SF3B1 knockdown in human CD34+ cells leads to increased apoptosis and cell cycle arrest of early-stage erythroid cells and generation of abnormally nucleated late-stage erythroblasts. RNA-seq analysis of SF3B1-knockdown erythroid progenitor CFU-E cells revealed altered splicing of an E3 ligase Makorin Ring Finger Protein 1 (MKRN1) and subsequent activation of p53 pathway.Decreased expression of genes involved in mitosis/cytokinesis pathway including polo-like kinase 1 (PLK1) was noted in SF3B1-knockdown polychromatic and orthochromatic erythroblasts comparing to control cells.

2021-04-24 | GSE173232 | GEO

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.

2015-04-22 | E-GEOD-65644 | biostudies-arrayexpress

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