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Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: cultured cells]

ABSTRACT: Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: cultured cells]

PROVIDER: PRJNA1019659 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26134071_1.fastq.gz	Fastqsanger.gz
	SRR26134071_2.fastq.gz	Fastqsanger.gz
	SRR26134072_1.fastq.gz	Fastqsanger.gz
	SRR26134072_2.fastq.gz	Fastqsanger.gz
	SRR26134073_1.fastq.gz	Fastqsanger.gz

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Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity

Project description:Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity

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Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [miRNA-seq]

Project description:Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [miRNA-seq]

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Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: dissected tissues]

Project description:Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: dissected tissues]

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Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: cultured cells]

Project description:Argonaute (AGO) proteins execute Micro-RNA (miRNA) mediated gene silencing. However it is currently debated whether all 4 mammalian AGO proteins (AGO1, AGO2, AGO3 and AGO4) are required for miRNA activity. To address this, we generated a mouse with deleted Ago1, Ago3 and Ago4 genes (Ago134), and found that these Argonaute proteins are completely redundant for miRNA biogenesis, miRNA homeostasis or miRNA function, a role that is carried out exclusively by AGO2. Instead, AGO1/3/4 are required to curtail the expansion of Type-2 adaptive immunity in mice via regulation of precursor-mRNA (pre-mRNA) splicing in CD4+ TH lymphocytes. Gain- and loss-of-function experiments demonstrate that nuclear AGO3 interacts directly with SF3B3, a component of the U2 spliceosome complex, to aid global mRNA splicing. Our work uncouples AGO1, AGO3 and AGO4 from miRNA-mediated RNAi, discovers a new AGO3:SF3B3 complex in the cellular nucleus, and reveals an underappreciated mechanism by which AGO proteins prevent hyper-inflammatory disease.

2024-10-31 | GSE243700 | GEO

Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [miRNA-seq]

2024-10-31 | GSE243916 | GEO

Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: dissected tissues]

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pre-mRNA splicing in C. elegans

Project description:pre-mRNA splicing in C. elegans

| PRJNA663456 | ENA

Competition between pre-mRNAs for a limiting splicing machinery drives global changes in splicing

Project description:During meiosis in yeast, global splicing efficiency increases. The mechanism for this is relief of competition for the splicing machinery by repression of intron-containing ribosomal protein genes (RPGs). Repression of RPGs with rapamycin also increases splicing efficiency in vegetative cells. Reducing levels of an RPG-dedicated transcription factor globally improves splicing and suppresses the temperature-sensitive growth defect of a spliceosome mutation. These results indicate that the spliceosome is limiting and pre-mRNAs compete with each other. Under these conditions, splicing efficiency of a given pre-mRNA therefore depends on both its concentration and affinity for the limiting splicing factor(s) as well as those of the competing pre-mRNAs. We propose that trans-competition control of splicing helps repress meiotic gene expression in vegetative cells, and promotes efficient meiosis. Competition between RNAs for a limiting factor may be a general condition important for function of a variety of post-transcriptional control mechanisms. Splicing and gene expression profiles of 1) wild type yeast cells treated with rapamycin (2 biological replicates) relative to untreated cells and 2) prp4-1 pGAL-IFH1 (down-regulated expression of IFH1 transcription factor(specific for ribosomal protein genes)) relative to prp4-1 yeast.

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CDK11 regulates pre-mRNA splicing by phosphorylation of SF3B1

Project description:RNA splicing, the process of intron removal from pre-mRNA, is essential for the regulation of gene expression. It is controlled by the spliceosome, a megadalton RNA-protein complex that assembles de novo on each pre-mRNA intron via an ordered assembly of intermediate complexes. Spliceosome activation is a major control step requiring dramatic protein and RNA rearrangements leading to a catalytically active complex. Splicing factor 3B subunit 1 (SF3B1) protein, a subunit of the U2 snRNP, is phosphorylated during spliceosome activation, but the responsible kinase has not been identified. Here we show that cyclin-dependent kinase 11 (CDK11) associates with SF3B1 and phosphorylates threonine residues at its N-terminus during spliceosome activation. The phosphorylation is important for association of SF3B1 with U5 and U6 snRNAs in spliceosome activated Bact complex and it can be blocked by OTS964, a potent and selective inhibitor of CDK11. CDK11 inhibition prevents spliceosomal transition from the precatalytic complex B to the activated complex Bact and leads to widespread intron retention and accumulation of non-functional spliceosomes on pre-mRNAs and chromatin. We characterize OTS964 as a quality chemical biology probe for CDK11 and demonstrate a central role of CDK11 in spliceosome assembly and splicing regulation.

2022-07-09 | MSV000089855 | MassIVE

An evolutionarily conserved function of the pre-mRNA splicing regulator TNPO3 for T cell development

Project description:All vertebrates possess lymphocytes, enabling the functional interrogation of this evolutionarily conserved organizing principle of adaptive immunity in non-mammalian species. A forward genetic screen in zebrafish indicated that a mutation of tnpo3, encoding a regulator of alternative splicing of pre-mRNAs, specifically impaired intrathymic T cell development. In mouse T cells, Tnpo3 deficiency predominantly disrupted the splicing of genes encoding RNA-binding motifs, and it specifically blocked the splicing of Va11, associated with reduced numbers of peripheral T cells and the complete loss of iNKT cells. Our results reveal an evolutionarily conserved function of a pre-mRNA processing factor for T cell development, uncovering a previously unappreciated checkpoint during the formation of mature mRNAs of the Tcra gene.

2019-01-23 | GSE77137 | GEO

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