Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA340948 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5099270.fastq.gz | Fastqsanger.gz | |||
| SRR5099280.fastq.gz | Fastqsanger.gz | |||
| SRR5099290.fastq.gz | Fastqsanger.gz | |||
| SRR5099271.fastq.gz | Fastqsanger.gz | |||
| SRR5099281.fastq.gz | Fastqsanger.gz |
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Project description:N6-methyladenosine (m6A) is the most abundant internal modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in cell differentiation and organism development. It regulates multiple steps throughout the RNA life cycle including RNA processing, translation, and metabolism, via the recognition by selective binding proteins. In cytoplasm, m6A binding protein YTHDF1 facilitates translation of m6A-modified mRNAs, and YTHDF2 accelerates the decay of m6A-modified transcripts. The biological function of YTHDF3, another cytoplasmic m6A binder of the YTH domain family, remains unknown. Here, we report that YTHDF3 promotes protein synthesis in synergy with YTHDF1, and affects methylated mRNA decay mediated by YTHDF2. Cells deficient in all of YTHDF proteins experience the most dramatic accumulation of the m6A-methylated transcripts. These results indicate that in cytoplasm, YTHDF proteins act in an integrated and cooperative network to accelerate metabolism of m6A-modified mRNAs. The combinative and dynamic nature of YTHDF proteins may collectively impact fundamental biological processes and diseases related to m6A RNA methylation.
2016-09-15 | GSE86214 | GEO
Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RIP-seq was conducted to investigate the occupancy of N6-methyladenosine RNA binding protein 3 (YTHDF3) served as “readers” that can recognize m6A modification site in HCT116 cells with oxaliplatin resistance (HCT116R). Then, YTHDF3 was knockdown by siRNA in HCT116 cells with oxaliplatin resistance, and RIP-seq was further conducted to investigate m6A methylation of HCT116, HCT116R and HCT116R cells with YTHDF3 knockdown.
2022-02-04 | E-MTAB-11321 | biostudies-arrayexpress
Project description:Knocking down YTHDF3 in breast cancer cells resulted in an altered gene expression profile N6-methyl-adenosine (m6A) is the most prevalent internal chemical modification in eukaryotic messenger RNAs and emerging as a critical mRNA chemical mark that mediates post-transcriptional gene expression regulation. YTHDF3 facilitates translation and decay of m6A-modified mRNAs. However, the role for YTHDF3 protein in breast cancer brain metastasis remain to be elucidated. We found that YTHDF3 is overexpressed in brain metastasis of breast cancer cells. Our study will characterize the expression profiling in YTHDF3 silencing breast cancer cells compared to shControl breast cancers cells. The objectives are to identify expression profiles that are specific to shYTHDF3 breast cancer cell to identify new the signaling pathway of YTHDF3 for brain metastasis of breast cancer cells.
2020-09-30 | GSE129946 | GEO
Project description:Knocking down YTHDF3 in breast cancer cells resulted in an altered gene expression profile N6-methyl-adenosine (m6A) is the most prevalent internal chemical modification in eukaryotic messenger RNAs and emerging as a critical mRNA chemical mark that mediates post-transcriptional gene expression regulation. YTHDF3 facilitates translation and decay of m6A-modified mRNAs. However, the role for YTHDF3 protein in breast cancer brain metastasis remain to be elucidated. We found that YTHDF3 is overexpressed in brain metastasis of breast cancer cells. Our study will characterize the expression profiling in YTHDF3 silencing breast cancer cells compared to shControl breast cancers cells. The objectives are to identify expression profiles that are specific to shYTHDF3 breast cancer cell to identify new the signaling pathway of YTHDF3 for brain metastasis of breast cancer cells.
2020-09-30 | GSE129945 | GEO
Project description:N6-methyladenosine Modulates Messenger RNA Translation Efficiency
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Project description:The variation of mRNA targets of mouse YTH N6-methyladenosine RNA binding protein 3 (Ythdf3) during nutrient starvation was determined by RNA immunoprecipitation and sequencing (RIP-seq).
2021-12-30 | GSE158660 | GEO
Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down
2015-06-09 | E-GEOD-63591 | biostudies-arrayexpress
Project description:During meiosis, in Saccharomyces cerevisiae, N6-methyladenosine (m6A) modified transcripts are induced, of which the function is unknown. Here, we uncover the role of the m6A reader Pho92. Cross-linking immunoprecipitation (CLIP) revealed that Pho92 associates with meiotic mRNAs in both m6A dependent and independent manner. Incidentally, Pho92 resides in the nucleus during early meiosis and associates with nascent RNAs, which is mediated through its interaction with Paf1C. Transcripts bound by Pho92 show elevated translational efficiency while cells lacking Pho92 display a small, but notable, increase in mRNA levels but not in protein levels, suggesting role of Pho92 in translation and decay. We show that Pho92 associates with ribosomes where it promotes the decay of m6A modified transcripts, contingent on active translation and the CCR4-NOT complex. We propose that m6A reader Pho92 is loaded co-transcriptionally to promote translation and subsequent decay fate of m6A modified transcripts, which ensures gamete fitness.
2022-12-06 | GSE193291 | GEO
Project description:Chemically modified mRNA nucleotides are emerging as key regulators of gene expression. Their effects are typically thought to be mediated through reader proteins that selectively bind to RNA molecules containing these modifications. Here, we present a new mechanism by which N6 methyladenosine (m6A) couples the translation of messenger RNA (mRNA) to its decay. m6A-modified codons are decoded inefficiently by the ribosome, rendering them “non-optimal”. At these codons, m6A slows down elongating ribosomes and thereby triggers translation-dependent decay of the mRNA. Inefficient decoding of m6A-modified codons is counteracted by the transfer RNA (tRNA) anticodon modification 5-methoxycarbonylmethyl-2-thiouridine (mcm5s2U). mcm5s2U increases the decoding efficiency of a subset of m6A codons and thereby alleviates m6A-mediated mRNA decay. This unanticipated link between the mRNA and tRNA epitranscriptomes controls the decay of mRNAs of important oncogenic signaling pathways. The biogenesis of m6A and mcm5s2U is coordinated in normal tissues but dysregulated in cancer, where a shift towards more mcm5s2U stabilizes these RNAs and is associated with higher tumor aggressiveness and poor prognosis. Thus, the balance between m6A and mcm5s2U acts as a pan-epitranscriptomic mechanism that regulates gene expression and curtails tumorigenesis.
2025-05-09 | GSE248503 | GEO
Project description:Chemically modified mRNA nucleotides are emerging as key regulators of gene expression. Their effects are typically thought to be mediated through reader proteins that selectively bind to RNA molecules containing these modifications. Here, we present a new mechanism by which N6 methyladenosine (m6A) couples the translation of messenger RNA (mRNA) to its decay. m6A-modified codons are decoded inefficiently by the ribosome, rendering them “non-optimal”. At these codons, m6A slows down elongating ribosomes and thereby triggers translation-dependent decay of the mRNA. Inefficient decoding of m6A-modified codons is counteracted by the transfer RNA (tRNA) anticodon modification 5-methoxycarbonylmethyl-2-thiouridine (mcm5s2U). mcm5s2U increases the decoding efficiency of a subset of m6A codons and thereby alleviates m6A-mediated mRNA decay. This unanticipated link between the mRNA and tRNA epitranscriptomes controls the decay of mRNAs of important oncogenic signaling pathways. The biogenesis of m6A and mcm5s2U is coordinated in normal tissues but dysregulated in cancer, where a shift towards more mcm5s2U stabilizes these RNAs and is associated with higher tumor aggressiveness and poor prognosis. Thus, the balance between m6A and mcm5s2U acts as a pan-epitranscriptomic mechanism that regulates gene expression and curtails tumorigenesis.
2025-05-09 | GSE248112 | GEO