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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE243918 | GEO | 2024/10/31

REPOSITORIES: GEO

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

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.

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

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The pre-mRNA retention and splicing complex controls expression of the Mediator subunit Med20.

Project description:The heterotrimeric pre-mRNA retention and splicing (RES) complex, consisting of Bud13p, Snu17p and Pml1p, promotes splicing and nuclear retention of a subset of intron-containing pre-mRNAs. Yeast cells deleted for individual RES genes show growth defects that are exacerbated at elevated temperatures. Although the growth phenotypes correlate to the splicing defects in the individual mutants, the underlying mechanism is unknown. Here, we show that the temperature sensitive (Ts) growth phenotype of bud13? and snu17? cells is a consequence of inefficient splicing of MED20 pre-mRNA, which codes for a subunit of the Mediator complex; a co-regulator of RNA polymerase II transcription. The MED20 pre-mRNA splicing defect is less pronounced in pml1? cells, explaining why they grow better than the other 2 RES mutants at elevated temperatures. Inactivation of the cytoplasmic nonsense-mediated mRNA decay (NMD) pathway in the RES mutants leads to accumulation of MED20 pre-mRNA, indicating that inefficient nuclear retention contributes to the growth defect. Further, the Ts phenotype of bud13? and snu17? cells is partially suppressed by the inactivation of NMD, showing that the growth defects are augmented by the presence of a functional NMD pathway. Collectively, our results demonstrate an important role of the RES complex in maintaining the Med20p levels.

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The pre-mRNA retention and splicing complex controls tRNA maturation by promoting TAN1 expression.

Project description:The conserved pre-mRNA retention and splicing (RES) complex, which in yeast consists of Bud13p, Snu17p and Pml1p, is thought to promote nuclear retention of unspliced pre-mRNAs and enhance splicing of a subset of transcripts. Here, we find that the absence of Bud13p or Snu17p causes greatly reduced levels of the modified nucleoside N(4)-acetylcytidine (ac(4)C) in tRNA and that a lack of Pml1p reduces ac(4)C levels at elevated temperatures. The ac(4)C nucleoside is normally found at position 12 in the tRNA species specific for serine and leucine. We show that the tRNA modification defect in RES-deficient cells is attributable to inefficient splicing of TAN1 pre-mRNA and the effects of reduced Tan1p levels on formation of ac(4)C. Analyses of cis-acting elements in TAN1 pre-mRNA showed that the intron sequence between the 5' splice site and branchpoint is necessary and sufficient to mediate RES dependency. We also show that in RES-deficient cells, the TAN1 pre-mRNA is targeted for degradation by the cytoplasmic nonsense-mediated mRNA decay pathway, indicating that poor nuclear retention may contribute to the tRNA modification defect. Our results demonstrate that TAN1 pre-mRNA processing has an unprecedented requirement for RES factors and that the complex controls the formation of ac(4)C in tRNA.

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Arabidopsis MOS4-associated complex promotes microRNA biogenesis and pre-mRNA splicing

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-12-06 | GSE103423 | GEO