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Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [Ribo-seq]

ABSTRACT: Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [Ribo-seq]

PROVIDER: PRJNA1109711 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28976200.fastq.gz	Fastqsanger.gz
	SRR28976201.fastq.gz	Fastqsanger.gz
	SRR28976196.fastq.gz	Fastqsanger.gz
	SRR28976197.fastq.gz	Fastqsanger.gz
	SRR28976198.fastq.gz	Fastqsanger.gz

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Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [Ribo-seq]

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

Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [RNA-Seq]

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Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [RNA-Seq]

Project description:Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [RNA-Seq]

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Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing to prevent double-stranded RNA accumulation

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

Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing to prevent double-stranded RNA accumulation

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Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [MeDIP-seq]

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.

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Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [RNA-seq]

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Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression

Project description:Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression

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RIP-Chip analysis supports different roles for AGO2 and GW182 proteins in recruiting and processing microRNA targets

Project description:RIP-Chip analysis supports different roles for AGO2 and GW182 proteins in recruiting and processing microRNA targets

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An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus [Ribo-seq, RNA-seq]

Project description:An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus [Ribo-seq, RNA-seq]

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