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METTL6 is a tRNA m3C methyltransferase that regulates translation and cell proliferation

ABSTRACT: METTL6 is a tRNA m3C methyltransferase that regulates translation and cell proliferation

PROVIDER: PRJNA605175 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11035076.fastq.gz	Fastqsanger.gz
	SRR11035077.fastq.gz	Fastqsanger.gz
	SRR11035078.fastq.gz	Fastqsanger.gz
	SRR11035079.fastq.gz	Fastqsanger.gz
	SRR11035082.fastq.gz	Fastqsanger.gz

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METTL6 is a tRNA m3C methyltransferase that regulates translation and cell proliferation

Project description:Here, we identified METTL6 as a bona fide tRNA methyltransferase, catalysing the formation of 3-methylcytidine (m3C) at C32 of specific serine tRNA isoacceptors. Accordingly, deletion of METTL6 in mouse stem cells results in changes in ribosome occupancy and RNA levels, as well as a spontaneous loss of pluripotency

2020-06-18 | GSE144866 | GEO

METTL6 is a tRNA m3C methyltransferase that regulates translation and tumor cell proliferation

Project description:METTL6 is a tRNA m3C methyltransferase that regulates translation and tumor cell proliferation

| PRJEB37209 | ENA

Epitranscriptomic regulation of cortical neural stem cell maintenance via Mettl8-dependent mitochondrial tRNA m3C modification

Project description:Increasing evidence implicates critical roles of various epitranscriptomic RNA modifications in different biological processes. Methyltransferase METTL8 installs 3-methylcytosine modification of mitochondrial tRNAs in vitro, however, its role in intact biological systems is completely unknown. Here we show that Mettl8 is localized in the mitochondria and installs m3C in mitochondrial tRNASer(UCN)/Thr in mouse embryonic cortical neural stem cells. At molecular and cellular levels, Mettl8 deletion in cortical neural stem cells leads to reduced mitochondrial protein translation and attenuated respiration activity. At the functional level, conditional Mettl8 deletion in mice results in impaired embryonic cortical neural stem cell maintenance in vivo, which can be rescued by pharmacologically enhancing mitochondrial functions. Similarly, METTL8 regulates mitochondrial protein expression and neural stem cell maintenance in human forebrain cortical organoids. Together, our study reveals a conserved epitranscriptomic mechanism of Mettl8 and mitochondrial tRNA m3C modification in maintaining embryonic cortical neural stem cells in mice and humans.

2023-01-12 | GSE214445 | GEO

m3C HAC-Seq analysis in HEK293T WT cells, METTL2A/2B knockout cells, METTL6 knockout cells, METTL2A/2B/6 knockout cells.

Project description:The ‘epitranscriptome’ includes a diversity of RNA modifications that influence gene expression. N3-methylcytidine (m3C) mainly occurs in the anticodon loop (position C32) of certain tRNAs yet its role is poorly understood. Here, using HAC-Seq, we report comprehensive METTL2A/B-, METTL6-, and METTL2A/B/6-dependent m3C profiles in human cells. METTL2A/B modifies most tRNA-Arginine and tRNA-Threonine members, whereas METTL6 modifies the tRNA-Serine family. However, decreased m3C32 on tRNA-Ser-GCT isodecoders was only observed with combined METTL2A/B/6 deletion. Ribo-Seq revealed altered translation of genes related to cell cycle and DNA repair pathways in METTL2A/2B/6-deficient cells, and these mRNAs are enriched in AGU codons that require tRNA-Ser-GCT for translation. These results, supported by reporter assays, help explain the observed slowed proliferation, altered cell cycle, and increased Cisplatin-sensitivity phenotypes of METTL2A/B/6-deficient cells. Thus, we define METTL2A/B/6-dependent methylomes and uncover a particular requirement of m3C tRNA modification for Serine codon-biased mRNA translation of cell cycle, and DNA repair genes.

2024-07-17 | GSE223469 | GEO

E-MTAB-8872

Project description:METTL6 is a tRNA m3C methyltransferase that regulates translation and tumor cell proliferation

2020-12-09 | E-MTAB-8872 | ExpressionAtlas

Nucleotide resolution profiling of m3C RNA modification by HAC-seq

Project description:We report a m3C-specific high-throughput sequencing techinque, Hydrazine-Aniline Cleavage sequencing (HAC-seq) to profile the m3C methylome at single-nucleotide resolution. We apply HAC-seq to analyze ribosomal RNA-depleted total RNA from MCF7 cells. We find that tRNA are the predominant m3C-modified RNA species. We find no evidence of m3C-modification of mRNA or other non-coding RNAs at comparable levels to tRNA in MCF7 cells.

2020-11-20 | GSE157682 | GEO

Ribosome Footprinting (RiboSeq) analysis of mRNA translation in HEK293T WT and METTL2A/2B/6 knockout cells

2024-07-17 | GSE223418 | GEO

METTL6 is a tRNA m3C methyltransferase that regulates translation and tumor cell proliferation

Project description:Transcriptome analysis of Mettl6 knockout embryonic stem cell lines to study the effect of METTL6 loss on pluripotency and self-renewal. Cell were cultured in standard serum+LIF media

2020-11-30 | E-MTAB-8872 | biostudies-arrayexpress

METTL1/WDR4 mediated tRNA N7-methylguanosine (m7G) modifications promote mRNA translation and lung cancer progression [TRAC-seq]

Project description:The tRNA N7-methylguanosine (m7G) modification is not essential for yeast growth, but in mammals mis-regulations of tRNA m7G modification cause stem cell defect and developmental disorders. Here we found that tRNA m7G methyltransferase complex components METTL1 and WDR4 are elevated in lung cancer tissues and associated with poor lung cancer prognosis. Functionally, depletion of METTL1 or WDR4 suppresses proliferation, migration, and invasion of lung cancer cells. In addition, forced expression of METTL1 or WDR4 promotes lung cancer progression depending on the tRNA m7G methyltransferase activity. Mechanistically, METTL1 knockdown leads to reduced tRNA m7G modification and decreased expression of m7G-modified tRNAs. Depletion of METTL1 selectively reduces the translation of a subset of oncogenic transcripts, including the genes related to cell proliferation in a m7G related codon dependent manner. Our study uncovered a new layer of translation regulation mechanism mediated by tRNA m7G modification, provided strong evidence to support the important physiological function of mis-regulated tRNA modification in cancer, and suggested that targeting METTL1 could be a promising strategy for lung cancer treatment.

2022-12-31 | GSE173760 | GEO

METTL1/WDR4 mediated tRNA N7-methylguanosine (m7G) modifications promote mRNA translation and lung cancer progression [RNA-seq]

2022-12-31 | GSE173750 | GEO