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METTL5 deficiency induces lung cancer regression via mitochondrial translation reduction

ABSTRACT: METTL5 deficiency induces lung cancer regression via mitochondrial translation reduction

PROVIDER: PRJNA1136550 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29849300.fastq.gz	Fastqsanger.gz
	SRR29849301.fastq.gz	Fastqsanger.gz
	SRR29849302.fastq.gz	Fastqsanger.gz
	SRR29849303.fastq.gz	Fastqsanger.gz
	SRR29849304.fastq.gz	Fastqsanger.gz

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METTL5 deficiency induces lung cancer regression via mitochondrial translation reduction

Project description:Cellular protein synthesis occurs through two types of translation: cytoplasmic and mitochondrial. These two types of translation operate independently but in coordination to regulate cell survival and death. Methyltransferase-like 5 (METTL5) has been found to play a role in directing the m6A modification of rRNA, which in turn controls cytoplasmic translation and impacts the decisions related to cell fate. In this study, we employed Ribo-seq to explore the effects of METTL5 deficiency on both cytoplasmic and mitochondrial translation.

2025-03-01 | GSE272389 | GEO

Mapping translation in wild-type and METTL5 knockout (KO) mice

Project description:We performed ribosome profiling on wild-type and METTL5 KO mice to investigate translation changes due to loss of METTL5.

2021-11-19 | GSE188798 | GEO

Mapping translation in wild-type and METTL5 knockout (KO) HepG2 cells

Project description:We performed ribosome profiling on wild-type and METTL5 KO HepG2 cells to investigate translation changes due to loss of METTL5.

2021-05-19 | GSE174419 | GEO

Loss of m6A methyltransferase METTL5 promotes cardiac hypertrophy through translational control of SUZ12

Project description:The methyltransferase-like5 (METTL5), which catalyzes m6A in 18S rRNA at position A1832, has been shown to regulate the efficient of mRNA translation in the differentiation of ES cell and the growth of cancer cells. It remains unknown that whether and how METTL5 regulates cardiac hypertrophy. In this study, we generated a mouse model (METTL5-cKO) with cardiac-specific abolishment of METTL5 in vivo. Loss function of METTL5 promotes pressure overload-induced cardiomyocyte hypertrophy and adverse remodeling. The regulatory function of METTL5 in hypertrophic growth of cardiomyocyte were further confirmed with both gain- and loss-of-function approaches in primary isolated cardiomyocytes. Mechanically, METTL5 was identified to modulate the mRNA translation of SUZ12, a core component of PRC2 complex, and further regulate the transcriptome shift during cardiac hypertrophy. Therefore, our study uncover an important translational regulator of cardiac hypertrophy.

2022-02-13 | GSE186615 | GEO

Mapping translation in wild-type and METTL5 knockout (KO) mice

Project description:Mapping translation in wild-type and METTL5 knockout (KO) mice

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RNA-seq and Ribo-seq of WT and METTL5 KO mECS.

Project description:Covalent chemical modifications of cellular RNAs directly impact all biological processes. However, our mechanistic understanding of the enzymes catalysing these modifications, their substrates and biological functions remains vague. Here, we undertook a systematic screen to uncover new RNA methyltransferases. We demonstrate that the methyltransferase-like 5 (METTL5) protein catalyses m6A in 18S rRNA at position A1832. We report that absence of Mettl5 in mouse embryonic stem cells (mESCs) results in a changes gene expression, decrease in translation rate, spontaneous loss of pluripotency and compromised differentiation potential. Mice lacking METTL5 recapitulate symptoms of patients with METTL5 mutations, thereby providing a new mouse disease model. Overall, our work highlights the importance of m6A in rRNA in stemness, differentiation, development and diseases.

2020-04-15 | GSE144313 | GEO

The rRNA m6A methyltransferase METTL5 is involved in pluripotency and developmental programmes

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Function and Mechanism of METTL5-mediated 18S rRNA m6A1832 modification in hepatocellular carcinoma

Project description:Tumor recurrence is main pattern of treatment failure for early-stage hepatocellular carcinoma (HCC). However, the molecular mechanisms underlying disease recurrence remain poorly understood. Here, we showed that 18S rRNA N6-methyladenosine (m6A1832) modification and its methyltransferase complex METTL5/TRMT112 were upregulated in HCC and correlated with poor prognosis. Loss-of-function and gain-of-function assays demonstrated that METTL5/TRMT112 mediated 18S rRNA m6A1832 modification promotes HCC tumorigenesis in vitro and in vivo. Mechanistically, 18S rRNA m6A1832 modification selectively regulated the translation of mRNAs with long 5’UTR and short 3’UTR through affecting the assembly of 80S subunit at translation initiation and its dissociation at translation termination which was executed by weakening the interaction of ABCE1 with eRF1 and eRF3. Moreover, METTL5-mediated 18S rRNA m6A1832 modification regulated β-oxidation of long-chain fatty acid through ACSL4 to promote HCC progression. Our work uncovered a novel layer of mRNA translation regulation mechanism at ribosome 80S subunit assembly and dissociation step mediated by 18S rRNA m6A1832 modification and revealed a new crosslink between RNA epigenetic modification and fatty acid metabolism in HCC.

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Identification of METTL5 interaction partners

Project description:METTL5 is an RNA methyltransferase whose stability was noted to be poor when expressed in both mammalian and bacterial expression systems. To determine if METTL5 has an endogenous stabilizing binding partner, FLAG-tagged METTL5 was expressed in Freestyle 293 cells and pulled down with anti-FLAG-M2 antibody-coupled magnetic beads. Bound proteins were fractionated by SDS-PAGE, and bands of interest were cut out for proteomics analysis.

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Mapping translation in wild-type and METTL5 knockout (KO) HepG2 cells

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