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E-MTAB-8872

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

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

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-8872-analysis-methods.tsv	Tabular
	E-MTAB-8872-analytics.tsv	Tabular
	E-MTAB-8872-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-8872-configuration.xml	Xml
	E-MTAB-8872-g3_g1-mvaPlot.png	Other

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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

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

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

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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

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

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

2024-07-17 | GSE223418 | GEO

E-MTAB-7451

Project description:Dis3L2 regulates cell proliferation and tissue growth through a conserved mechanism

2021-01-19 | E-MTAB-7451 | ExpressionAtlas

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

E-GEOD-55077

Project description:Nkx6.1 regulates islet beta-cell proliferation via Nr4a1 and Nr4a3 nuclear receptors

2015-08-04 | E-GEOD-55077 | ExpressionAtlas

METTL1/WDR4-mediated tRNA m7G modification and mRNA translation control promotes oncogenesis and doxorubicin resistance in osteosarcoma

Project description:Osteosarcoma is the most common bone tumor that leads to high mortality in adolescents and children. The tRNA N7-methylguanosine methyltransferase METTL1 is located in chromosome 12q14.1, a region that is frequently amplified in osteosarcoma patients, while its functions and underlying mechanisms in regulation of osteosarcoma remain unknown. Herein we show that METTL1 and WDR4 are overexpressed in osteosarcoma and associated with poor patient prognosis. Knockdown of METTL1 or WDR4 causes decreased tRNA m7G modification level and impairs osteosarcoma progression in vitro and in vivo. Conversely, METTL1/WDR4 overexpression promotes osteosarcoma proliferation, migration and invasion capacities. tRNA methylation and mRNA translation profiling indicated that METTL1/WDR4 modified tRNAs enhance translation of mRNAs with more m7G tRNA-decoded codons, including extracellular matrix (ECM) remodeling effectors, which facilitates osteosarcoma progression and chemoresistance to doxorubicin.Our study demonstrates METTL1/WDR4 mediated tRNA m7G modification plays crucial oncogenic functions to enhance osteosarcoma progression and chemoresistance to doxorubicin via alteration of oncogenic mRNA translation, suggesting METTL1 inhibition combined with chemotherapy is a promising strategy for treatment of osteosarcoma patients.

2024-02-01 | GSE225515 | GEO

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