M6A/m-Seq of mouse adult cortex after acute stress
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA453975 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7074300_1.fastq.gz | Fastqsanger.gz | |||
| SRR7074300_2.fastq.gz | Fastqsanger.gz | |||
| SRR7074310_1.fastq.gz | Fastqsanger.gz | |||
| SRR7074310_2.fastq.gz | Fastqsanger.gz | |||
| SRR7074320_1.fastq.gz | Fastqsanger.gz |
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Project description:N6-Methyladenosine (m6A) and N6,2′-O-dimethyladenosine (m6Am) are abundant mRNA modifications that regulate transcript processing and translation. The role of both, here termed m6A/m, in the stress response in the adult brain in vivo are currently unknown. Here, we provide a detailed analysis of the stress-epitranscriptome using m6A/m-Seq of 10-12 w male C57BL/6 mouse cortex of unstressed or acutely stressed mice (4 h after 15 min restraint stress) of 6-7 samples per condition (pooled from 3 mice each). PolyA-RNA-fragments of each sample was processed both as m6A/m-sample (RNA immunoprecipiation RIP with an m6A and m6Am antibody) and RNA-input sample.
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Project description:N6-Methyladenosine (m6A) and N6,2′-O-dimethyladenosine (m6Am) are abundant mRNA modifications that regulate transcript processing and translation. The role of both, here termed m6A/m, in the stress response in the adult brain in vivo are currently unknown. Here, we provide ribosome profiling data of 10-12 w male C57BL/6 mouse cortex of unstressed or acutely stressed mice (4 h after 15 min restraint stress) of 6 samples per condition to relate to m6A/m-Seq data of similiar samples.
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Project description:N6-Methyladenosine (m6A) and N6,2′-O-dimethyladenosine (m6Am) are abundant mRNA modifications that regulate transcript processing and translation. The role of both, here termed m6A/m, in the stress response in the adult brain in vivo are currently unknown. Here, we investigated the effect of gene deletion of Mettl3, a m6A methyltransferase, and Fto, a m6A and m6Am demethlyase, induced in adulthood in excitatory neurons of the neocortex and hippocampus (Camk2a-Cre Mettl3 or Fto cKO) on the cortical epitranscriptome. PolyA-RNA-fragments from 3-5 replicates per group were processed both as m6A/m-sample (RNA immunoprecipiation RIP with an m6A and m6Am antibody) and RNA-input sample.
2018-07-10 | GSE113793 | GEO
Project description:N6-methyladenosine (m6A) is one of the most prevalent and conserved RNA modifications. It controls several biological processes, including the biogenesis and function of circular RNAs (circRNAs), which are a class of covalently closed-single stranded RNAs. Several studies have revealed that proteotoxic stress response induction could be a relevant anticancer therapy in Acute Myeloid Leukemia (AML). Furthermore, it has emerged a strong molecular interaction between the m6A mRNA modification factors and the suppression of the proteotoxic stress response. Since the proteasome inhibition leading to the imbalance in protein homeostasis is strictly linked to the stress response induction, we investigated the role of Bortezomib (Btz) on m6A regulation and in particular its impact on the modulation of m6A-dependent circRNAs expression. Here, we show that the treatment of AML cells with Btz downregulated the expression of the m6A regulator WTAP at translational level, mainly because of increased oxidative stress. Indeed, Btz treatment promoted oxidative stress, with ROS generation and HMOX-1 activation and administration of the reducing agent N-acetylcysteine restored WTAP expression. Additionally, we identified m6A-modified circRNAs modulated by Btz treatment, including circHIPK3, which is implicated in protein folding and oxidative stress regulation upon silencing. These results highlight the intricate molecular networks involved in oxidative and ER stress induction in AML cells following proteotoxic stress response, laying the groundwork for future therapeutic strategies targeting these pathways.
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Project description:The mRNA m6A reader YTHDF2 is overexpressed in a broad spectrum of human acute myeloid leukemias (AML). To understand the role of YTHDF2 in AML, we generated m6A meRIP-seq libraries form Ythdf2fl/fl (Ythdf2CTL) pre-leukemic cells.
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