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TRNA 2’-O-methylation by a duo of TRM7/FTSJ1 proteins modulates small RNA silencing in Drosophila.

ABSTRACT: tRNA 2’-O-methylation by a duo of TRM7/FTSJ1 proteins modulates small RNA silencing in Drosophila.

PROVIDER: PRJNA554844 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9693305_1.fastq.gz	Fastqsanger.gz
	SRR9693305_2.fastq.gz	Fastqsanger.gz
	SRR9693306_1.fastq.gz	Fastqsanger.gz
	SRR9693306_2.fastq.gz	Fastqsanger.gz
	SRR9693307_1.fastq.gz	Fastqsanger.gz

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tRNA 2’-O-methylation by a duo of TRM7/FTSJ1 proteins modulates small RNA silencing in Drosophila.

Project description:tRNA 2’-O-methylation by a duo of TRM7/FTSJ1 proteins modulates small RNA silencing in Drosophila.

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tRNA 2’-O-methylation by a duo of TRM7/FTSJ1 proteins modulates small RNA silencing in Drosophila.

Project description:2’-O-methylation (Nm) represents one of the most common RNA modifications. Nm affects RNA structure and function with crucial roles in various RNA-mediated processes ranging from RNA silencing, translation, self versus non-self recognition to viral defense mechanisms. Here, we identify two novel Nm methyltransferases (Nm-MTases) in Drosophila melanogaster (CG7009 and CG5220) as functional orthologs of yeast TRM7 and human FTSJ1. Genetic knockout studies together with MALDI-TOF mass spectrometry and RiboMethSeq mapping revealed that CG7009 is responsible for methylating the wobble position in tRNAPhe, tRNATrp and tRNALeu, while subsequently, CG5220 methylates position C32 in the same tRNAs and targets also additional tRNAs. CG7009 or CG5220 mutant animals were viable and fertile but exhibited various phenotypes such as life span reduction, small RNA pathways dysfunction and increased sensitivity to RNA virus infections. Our results provide the first detailed characterization of two TRM7 family members in Drosophila and uncover a molecular link between enzymes catalysing Nm at specific tRNAs and small RNA-induced gene silencing pathways.

2020-01-03 | GSE134354 | GEO

tRNA 2'-O-methylation by a duo of TRM7/FTSJ1 proteins modulates small RNA silencing in Drosophila.

Project description:2'-O-Methylation (Nm) represents one of the most common RNA modifications. Nm affects RNA structure and function with crucial roles in various RNA-mediated processes ranging from RNA silencing, translation, self versus non-self recognition to viral defense mechanisms. Here, we identify two Nm methyltransferases (Nm-MTases) in Drosophila melanogaster (CG7009 and CG5220) as functional orthologs of yeast TRM7 and human FTSJ1. Genetic knockout studies together with MALDI-TOF mass spectrometry and RiboMethSeq mapping revealed that CG7009 is responsible for methylating the wobble position in tRNAPhe, tRNATrp and tRNALeu, while CG5220 methylates position C32 in the same tRNAs and also targets additional tRNAs. CG7009 or CG5220 mutant animals were viable and fertile but exhibited various phenotypes such as lifespan reduction, small RNA pathways dysfunction and increased sensitivity to RNA virus infections. Our results provide the first detailed characterization of two TRM7 family members in Drosophila and uncover a molecular link between enzymes catalyzing Nm at specific tRNAs and small RNA-induced gene silencing pathways.

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selenocysteine tRNA methylation promotes oxidative stress resistance in melanoma metastasis

Project description:Oxidative stress has been shown to limit metastasis of numerous cancer types including melanoma. A specialized group of 25 proteins containing the 21st amino acid, selenocysteine, plays a central role in oxidative stress resistance, which is a key driver of metastasis. A single selenocysteine tRNA methylation, Um34, is required for the translation of several stress-related selenoproteins in a selenium-dependent manner. Herein, we characterize FTSJ1 as the Um34 methyltransferase and show that its activity is required for the Sec tRNA (tRNASec) Um34 modification. Loss of Um34 affects translation of a subset of selenoproteins and increases melanoma cell sensitivity to oxidative stress while increased Um34 levels promote oxidative stress resistance. Loss of FTSJ1 does not affect primary melanoma tumor growth but abolishes metastatic spread in vivo. Overexpression of FTSJ1 specifically increases melanoma metastasis in vivo. Our work establishes FTSJ1 as the Um34 methyltransfearse and tRNASec Um34 modification as a central regulator of oxidative stress resistance during melanoma metastasis.

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8-week WT or Ftsj1 KO mouse brain tRNA and tRF MiSeq

Project description:8-week WT or Ftsj1 KO mouse brain tRNA and tRF MiSeq

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FTSJ1 patients RNASeq

Project description:RNASeq: FTSJ1 tRNA Nm-MTase: new human targets and role in the regulation of brain-specific genes

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FTSJ1 patients RiboMethSeq

Project description:RiboMethSeq FTSJ1 tRNA Nm-MTase: new human targets and role in the regulation of brain-specific genes

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