Arabidopsis MOS4-associated complex promotes microRNA biogenesis and pre-mRNA splicing
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA401314 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5462340.fastq.gz | Fastqsanger.gz | |||
| SRR5462341.fastq.gz | Fastqsanger.gz | |||
| SRR5462342.fastq.gz | Fastqsanger.gz | |||
| SRR5462335.fastq.gz | Fastqsanger.gz | |||
| SRR5462336.fastq.gz | Fastqsanger.gz |
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Project description:The evolutionarily conserved, putative RNA helicase MAC7 exists in both animals and plants. The human MAC7 homolog, Aquarius, is part of the spliceosome and plays a role in pre-mRNA splicing in vitro. In Arabidopsis, MAC7 was shown to be part of the MOS4-associated complex (MAC), which is required for plant defense and development. Here through RNA-seq analysis we discover that down-regulated genes in MAC subunit mutants are mostly involved in plant defense and stimulus response, confirming a role of MAC in the regulation of biotic and abiotic stress responses. We also discover global intron retention defects in mutants in three members of MAC, thus linking the functions of MAC to splicing in Arabidopsis. In addition, we show that mac7-1, a partial loss-of-function mutant in MAC7, and two other MAC subunit mutants, mac3a mac3b and prl1 prl2, exhibit reduced microRNA levels in general, indicating that MAC promotes microRNA biogenesis. The mac7-1 mutant shows reduced primary miRNA (pri-miRNA) levels without affecting MIR promoter activity or the degradation of pri-miRNA transcripts, implicating functions of MAC7 during transcription elongation or maturation of pri-miRNAs. As a nuclear protein, MAC7 is not localized in dicing bodies, but it affects the localization of HYL1 to dicing bodies. We propose that MAC acts to link MIR transcription to pri-miRNA processing.
2017-12-08 | GSE98035 | GEO
Project description:The evolutionarily conserved, putative RNA helicase MAC7 exists in both animals and plants. The human MAC7 homolog, Aquarius, is part of the spliceosome and plays a role in pre-mRNA splicing in vitro. In Arabidopsis, MAC7 was shown to be part of the MOS4-associated complex (MAC), which is required for plant defense and development. Here through RNA-seq analysis we discover that down-regulated genes in MAC subunit mutants are mostly involved in plant defense and stimulus response, confirming a role of MAC in the regulation of biotic and abiotic stress responses. We also discover global intron retention defects in mutants in three members of MAC, thus linking the functions of MAC to splicing in Arabidopsis. In addition, we show that mac7-1, a partial loss-of-function mutant in MAC7, and two other MAC subunit mutants, mac3a mac3b and prl1 prl2, exhibit reduced microRNA levels in general, indicating that MAC promotes microRNA biogenesis. The mac7-1 mutant shows reduced primary miRNA (pri-miRNA) levels without affecting MIR promoter activity or the degradation of pri-miRNA transcripts, implicating functions of MAC7 during transcription elongation or maturation of pri-miRNAs. As a nuclear protein, MAC7 is not localized in dicing bodies, but it affects the localization of HYL1 to dicing bodies. We propose that MAC acts to link MIR transcription to pri-miRNA processing.
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Project description:Arabidopsis MOS4-associated complex promotes microRNA biogenesis and pre-mRNA splicing [RNA-seq]
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Project description:Arabidopsis MOS4-associated complex promotes microRNA biogenesis and pre-mRNA splicing [ncRNA-seq]
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Project description:Biogenesis of eukaryotic messenger ribonucleoprotein complexes (mRNPs) involves the synthesis, splicing, and 3M-bM-^@M-^Y-processing of pre-mRNA, and the assembly of mature mRNPs for nuclear export. We mapped 23 mRNP biogenesis factors onto the newly synthesized yeast transcriptome, providing ~10^5-10^6 high-confidence RNA interaction sites per factor. PAR-CLIP data of 23 mRNP biogenesis factors in Saccharomyces cerevisiae
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2024-10-31 | GSE243916 | GEO
Project description:Pre-mRNA splicing requires assembly of spliceosome that consists of hundreds of factors forming various dynamic complexes with or without small nuclear RNAs (snRNAs). Systematic identification of the splicing factors remains a significant challenge especially in vivo. In our genetic screening for the factors required for division asynchrony during Caenorhabditis elegans embryogenesis, we identified a highly conserved but uncharacterized essential protein, GAD-1, that is necessary for setting cell cycle length of intestine progenitors, a function that is shared with many other factors involved in transcription, pre-mRNA splicing or polyadenylation, suggesting its potential role in mRNA biogenesis. Co-immunoprecipitation followed by mass spectrometry reveals that GAD-1 mainly interacts with non-snRNP type of splicing complex called NineTeen Complex (NTC). Consistent with this, RNA-seq analysis demonstrates pervasive defects in pre-mRNA splicing in gad-1 mutants. Transgenic reporter assay shows its ubiquitous and nuclear expression across developmental stages. Immunostaining of the C-terminal domain of RNA polymerase II demonstrates a GAD-1’s role in transcription elongation. In agreement with this, depletion of GAD-1 and its interacting partners inhibits expression of both ubiquitous and tissue-specific genes, supporting that both GAD-1 and many of its interacting proteins are novel components of NTC or its associated spliceosome. Taken together, we identify GAD-1 and its multiple interacting partners as novel components of spliceosome in vivo through which they regulate pre-mRNA splicing and transcription elongation.
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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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