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Polysome profiling RNA seq experiments on extracts from METTL3-WT and METTL3-K177Q reconstituting cells

ABSTRACT: polysome profiling RNA seq experiments on extracts from METTL3-WT and METTL3-K177Q reconstituting cells

PROVIDER: PRJNA758823 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15667527_1.fastq.gz	Fastqsanger.gz
	SRR15667527_2.fastq.gz	Fastqsanger.gz
	SRR15667528_1.fastq.gz	Fastqsanger.gz
	SRR15667528_2.fastq.gz	Fastqsanger.gz
	SRR15667529_1.fastq.gz	Fastqsanger.gz

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polysome profiling RNA seq experiments on extracts from METTL3-WT and METTL3-K177Q reconstituting cells

Project description:Given the overall steady-state mRNA abundance between these two groups displayed negligible differences, these data implied an increased translational efficiency in cells bearing K177Q mutation.

2022-09-20 | GSE183016 | GEO

m6A methylome in WT- and K177Q-METTL3 reconstituting MDA-MB-231 cells as well as in METTL3-deficient MDA-MB-231 cells.

Project description:We report the application of MeRIP sequencing technology for high-throughput profiling of m6A methylome in breast cancer cells. Comparison of m6A methylome between METTL3-WT and METTL3-K177Q reconstituting cells revealed the following findings: 1) Significant global alteration of methylation sites due to K177Q mutation (termed as KQ-m6A signature). 2) GO analysis of the differential m6A-MeRIP candidates enriched pathways involved in chromatin modification, RNA splicing, DNA damage, cell cycle, and autophagy, consistent with a critical role of m6A-mediated nuclear biological activities and highlighted generally recognized cellular events associated with tumorigenesis. 3) we dissected potential mechanistic clues explaining the attenuated invasive phenotype in METTL3K177Q reconstituting cells.

2022-09-20 | GSE183014 | GEO

m6A methylome in WT- and K177Q-METTL3 reconstituting MDA-MB-231 cells as well as in METTL3-deficient MDA-MB-231 cells.

Project description:m6A methylome in WT- and K177Q-METTL3 reconstituting MDA-MB-231 cells as well as in METTL3-deficient MDA-MB-231 cells.

| PRJNA758813 | ENA

METTL3 promotes translation in human cancer cells

Project description:we find METTL3 associates with polyribosomes and promotes translation. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to the 3' untranslated region (UTR) of a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through an interaction with the translation initiation machinery. m6A seq in A549 and H1299 cells, RNA seq in METTL3 knockdown cells

2016-07-03 | E-GEOD-76367 | biostudies-arrayexpress

Expression & polysome association in pluripotent human embryonic stem cells

Project description:The goal was to measure the expression and polysome association of genes with polysomes in human embryonic stem cells H9 human embryonic stem cells were kept in pluripotent conditions. Total RNA and polysome extracts were isolated.

2012-09-01 | E-GEOD-31768 | biostudies-arrayexpress

METTL3 KD in HepG2 cells

Project description:To gain insight into possible processes that require m6A for their function, METTL3 was knocked down (KD) in HepG2 cells by siRNA transfections Differential expression analysis of METTL3 KD versus mock-transfected HepG2 cells, in 2 biological replicates

2012-04-25 | E-GEOD-37001 | biostudies-arrayexpress

BET inhibition abrogates global transcription via repressing m6A writer complex

Project description:To characterize the role of m6A modification in mediating BRD4-dependent biological functions, we established METTL3 reconstituting cells and treated with JQ1 BRD4 directs gene transcription through diverse mechanisms. Here, we specifically focused on BETi-dependent transcriptome or chestrated by m6A-mediated regulation. To this end, we first need to identify bona fide m6A-dependent transcripts via rescue experiments in METTL3-knockdown cells by adding back wild-type METTL3 or METTL3-CD mutant (a catalytically inactive form of METTL3)

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Binding motif analysis of METTL3，WTAP in METTL3，WTAP overexpressed Human 293T cells

Project description:label the cells overexpressed Myc tagged METTL3 and Flag tagged WTAP with 4-SU, the RNA bound by METT3,WTAP can be got by Myc or Flag IP followed by RNA isolation by using the TRIzol (Invitrogen) reagent by following the company manual.the RNA was then used for library preparation using a TruSeq™ RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturer’s protocol.The libraries were sequenced using HiSeq2000 (Illumina) in single-read mode, creating reads with a length of 50 bp. Sequencing chemistry v2 (Illumina) was used and samples were multiplexed in two samples per lane. discovery of the binding motif of METTL3，WTAP in METTL3，WTAP overexpressed Human 293T cells

2014-01-16 | E-GEOD-50580 | biostudies-arrayexpress

METTL3 preferentially enhances non-m6A translation of epigenetic factors and promotes tumorigenesis (meRIP, RIP and polysome-seq)

Project description:Methyltransferase-like 3 (METTL3) is the best known m6A methyltransferase of the N6-adenosine-methyltransferase complex that functions in the reversible epi-transcriptome modulation of m6A modification. Besides acting as a m6A methyltransferase, METTL3 also regulates mRNA translation as well as other biological processes either through m6A “reader”-mediated downstream effect or directly binding to m6A sites, but the underlying mechanism and biological significance of these cytoplasmic events remain undefined. Here, we demonstrated that METTL3 inhibition significantly delayed gastric tumorigenesis in patient-derived xenograft model. Intriguingly, global METTL3-binding profiling revealed METTL3 occupied numerous oncogenic mRNAs without m6A signals, indicating a novel mechanism independent of m6A machinery. Furthermore, METTL3 was observed to translocate from nucleus to cytoplasm during gastric carcinogenesis, and its cytoplasm-to-nucleus ratio was correlated with cancer progression. In addition, the nuclear retention of METTL3 nearly abolished its tumor-promoting activity. Mechanistically, METTL3 interacted with PABPC1 to promote RNA looping, thus facilitating the translation of multiple oncogenic mRNAs. Taken together, our findings indicate an unexpected role of METTL3 as an important translational regulator independent of either m6A-“writer” or -“reader” activities and suggest METTL3 as a therapeutic target in gastric cancer.

2022-05-16 | GSE163310 | GEO

METTL3-WT and METTL3-K177Q

Project description:METTL3-WT and METTL3-K177Q

| PRJNA758816 | ENA