Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [RNA-Seq]
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ABSTRACT:
PROVIDER: PRJNA1109712 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28976190.fastq.gz | Fastqsanger.gz | |||
| SRR28976191.fastq.gz | Fastqsanger.gz | |||
| SRR28976192.fastq.gz | Fastqsanger.gz | |||
| SRR28976193.fastq.gz | Fastqsanger.gz | |||
| SRR28976194.fastq.gz | Fastqsanger.gz |
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Project description:Mitochondrial biogenesis relies on both the nuclear and mitochondrial genomes, and imbalance in their expression can lead to inborn errors of metabolism, inflammation, and aging. Here, we investigate N6AMT1, a nucleo-cytosolic methyltransferase that exhibits genetic codependency with mitochondria. We determine transcriptional and translational profiles of N6AMT1 and report that it is required for the cytosolic translation of TRMT10C (MRPP1) and PRORP (MRPP3), two subunits of the mitochondrial RNAse P enzyme. In the absence of N6AMT1, or when its catalytic activity is abolished, RNA processing within mitochondria is impaired, leading to the accumulation of unprocessed and double-stranded RNA, thus preventing mitochondrial protein synthesis and oxidative phosphorylation, and leading to an immune response. Our work sheds light on the function of N6AMT1 in protein synthesis and highlights a cytosolic program required for proper mitochondrial biogenesis.
2024-11-11 | GSE267077 | GEO
Project description:Mitochondrial biogenesis relies on both the nuclear and mitochondrial genomes, and imbalance in their expression can lead to inborn errors of metabolism, inflammation, and aging. Here, we investigate N6AMT1, a nucleo-cytosolic methyltransferase that exhibits genetic codependency with mitochondria. We determine transcriptional and translational profiles of N6AMT1 and report that it is required for the cytosolic translation of TRMT10C (MRPP1) and PRORP (MRPP3), two subunits of the mitochondrial RNAse P enzyme. In the absence of N6AMT1, or when its catalytic activity is abolished, RNA processing within mitochondria is impaired, leading to the accumulation of unprocessed and double-stranded RNA, thus preventing mitochondrial protein synthesis and oxidative phosphorylation, and leading to an immune response. Our work sheds light on the function of N6AMT1 in protein synthesis and highlights a cytosolic program required for proper mitochondrial biogenesis.
2024-11-11 | GSE267078 | GEO
Project description:Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [Ribo-seq]
| PRJNA1109711 | ENA
Project description:Mitochondrial biogenesis relies on both the nuclear and the mitochondrial genomes, and the mechanisms that support their coordinated expression are not fully understood. Improper mitochondrial DNA expression can lead to inborn error of metabolism, inflammation, and aging. Here, we investigate N6AMT1, a nucleo-cytosolic multi-substrate methyltransferase. We analyze genetic dependency, transcription, translation, and proteomic profiles of N6AMT1-depleted cells and report that N6AMT1 is necessary for the cytosolic translation of factors involved in mitochondrial RNA metabolism, including subunits of the mitochondrial RNase P. In the absence of N6AMT1, RNA processing and translation within mitochondria are impaired, while double-stranded RNA accumulates in mitochondrial RNA granules causing an interferon response. Our work highlights a cytosolic program required for proper mitochondrial biogenesis, with consequences on innate immunity.
2024-11-11 | PXD051311 | Pride
Project description:Mitochondrial biogenesis relies on both the nuclear and the mitochondrial genomes, and the mechanisms that support their coordinated expression are not fully understood. Improper mitochondrial DNA expression can lead to inborn error of metabolism, inflammation, and aging. Here, we investigate N6AMT1, a nucleo-cytosolic multi-substrate methyltransferase. We analyze genetic dependency, transcription, translation, and proteomic profiles of N6AMT1-depleted cells and report that N6AMT1 is necessary for the cytosolic translation of factors involved in mitochondrial RNA metabolism, including subunits of the mitochondrial RNase P. In the absence of N6AMT1, RNA processing and translation within mitochondria are impaired, while double-stranded RNA accumulates in mitochondrial RNA granules causing an interferon response. Our work highlights a cytosolic program required for proper mitochondrial biogenesis, with consequences on innate immunity.
2024-11-06 | PXD051180 | Pride
Project description:Background: DNA N6-methyladenosine (6mA) as a novel epigenetic signaling modification in humans and has been implicated in progression and tumorigenesis of several cancers. However, the function and mechanisms of 6mA in breast cancer (BC), the most common cancer among women, are unclear. Methods: The clinical role of 6mA was investigated by immunohistochemical (IHC) staining and Kaplan-Meier analysis of BC and their normal tissues. 6mA immunoprecipitation (IP) sequencing, mRNA sequencing and bioinformatics analysis were used to screen and validate the direct targets of 6mA. Results: Decreases in N6AMT1 correlated with the extent of 6mA in BC tissues and predicted a worse overall survival of BC patients. Knockdown N6AMT1 markedly reduced 6mA in DNA and promoted the proliferation and migration of BC in vivo and in vitro, whereas overexpression of N6AMT1 had the opposite effect, indicating N6AMT1 is a functional methyltransferase for DNA 6mA and relates with gene transcription. Critical negative regulators of the cell cycle, such as RB1, P21, REST and TP53 were identified as targets of N6AMT1 in BC. Conclusion: These results suggest N6AMT1 enhances DNA 6mA levels to repress tumor progression via transcriptional regulation of cell cycle inhibitors.
2022-03-31 | GSE166576 | GEO
Project description:Background: DNA N6-methyladenosine (6mA) as a novel epigenetic signaling modification in humans and has been implicated in progression and tumorigenesis of several cancers. However, the function and mechanisms of 6mA in breast cancer (BC), the most common cancer among women, are unclear. Methods: The clinical role of 6mA was investigated by immunohistochemical (IHC) staining and Kaplan-Meier analysis of BC and their normal tissues. 6mA immunoprecipitation (IP) sequencing, mRNA sequencing and bioinformatics analysis were used to screen and validate the direct targets of 6mA. Results: Decreases in N6AMT1 correlated with the extent of 6mA in BC tissues and predicted a worse overall survival of BC patients. Knockdown N6AMT1 markedly reduced 6mA in DNA and promoted the proliferation and migration of BC in vivo and in vitro, whereas overexpression of N6AMT1 had the opposite effect, indicating N6AMT1 is a functional methyltransferase for DNA 6mA and relates with gene transcription. Critical negative regulators of the cell cycle, such as RB1, P21, REST and TP53 were identified as targets of N6AMT1 in BC. Conclusion: These results suggest N6AMT1 enhances DNA 6mA levels to repress tumor progression via transcriptional regulation of cell cycle inhibitors.
2022-03-31 | GSE166580 | GEO
Project description:The RNA exosome is a key 3’-5’ exoribonuclease with evolutionary conserved structure and roles. Its cytosolic functions require the co-factors SKI7 and the Ski complex. Here we demonstrate by co-purification experiments that the ARM repeat protein RESURRECTION1 (RST1) and RST1 INTERACTING PROTEIN (RIPR) connect the cytosolic Arabidopsis RNA exosome to the Ski complex. rst1 and ripr mutants accumulate small RNAs many of which are quality control siRNAs (rqc-siRNAs) produced by the postranscriptional gene silencing (PTGS) machinery when mRNA degradation is compromised. Indeed, quasi identical small RNA populations are observed in mutants lacking the RRP45B/CER7 subunit of the core exosome. This biochemical and genetic evidence supports a physical and functional link between RST1, RIPR and the RNA exosome. Our data reveal the existence of additional cytosolic exosome co-factors besides the known SKI subunits. Interestingly, RST1 is not restricted to plants, as homologues with a similar domain architecture exist in animals, including humans.
2019-07-17 | PXD013435 | Pride
Project description:Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [RNA-seq]
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Project description:mRNA processing is critical for gene expression. A challenge in regulating mRNA processing is how to recognize the actual mRNA processing sites such as splice sites and polyadenylation sites when the sequence content is insufficient for this purpose. Previous studies suggested that RNA structure affects mRNA processing. However, the regulatory role of RNA structure in mRNA processing remains unclear. Here, we performed in vivo SHAPE chemical profiling on Arabidopsis nuclear RNAs and generated the in vivo nuclear RNA structure landscape. We found that nuclear mRNAs fold differently from cytosolic mRNAs. Notably, we discovered a two-nucleotide single-stranded RNA structure feature upstream of 5’ splice site that regulates splicing and is responsible for the selection of alternative 5’ splice sites. Moreover, we found branch point single-strandedness is associated with 3’ splice site recognition. We also identified an RNA structure feature comprising two close-by single-stranded regions that is specifically associated with both polyadenylation and alternative polyadenylation events. Our work demonstrates an RNA structure regulatory mechanism for mRNA processing.
2020-12-10 | GSE135711 | GEO