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RNA expression analysis after RNA polymerase II transcriptional blocking with α-amanitin

ABSTRACT: Transcriptional profiling of HeLa cells treated with α-amanitin for 9 h. Relative abundance to untreated control cells was used to evaluate the biogenesis of lncRNAs by RNA polymerase II.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62989 | GEO | 2015/06/30

SECONDARY ACCESSION(S): PRJNA266345

REPOSITORIES: GEO

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RNA expression analysis after RNA polymerase II transcriptional blocking with α-amanitin

Project description:Transcriptional profiling of HeLa cells treated with α-amanitin for 9 h. Relative abundance to untreated control cells was used to evaluate the biogenesis of lncRNAs by RNA polymerase II. Two-condition experiment, alpha-amanitin-treated vs. untretated HeLa cells. Biological replicates: 4 with dye-swap

2015-06-30 | E-GEOD-62989 | biostudies-arrayexpress

Transcription profiling of Xenopus laevis early gastrulation embryos injected with alpha-amanitin against RNA polymerase II activity

Project description:Xenopus laevis embryos were injected with alpha-amanitin to inhibit RNA polymerase II activity. Embryos were allowed to develop up to stage 10.5 (early gastrula, control and alpha-amanitin injected embryos) and subsequently collected for RNA isolation. The transcriptome profiles of alpha-amanitin injected and control embryos were compared.

2016-03-07 | E-MTAB-3614 | biostudies-arrayexpress

Alpha-amanitin treatment effect on intronic transcription

Project description:We compared the gene expression profiles of prostate carcinoma cells, LNCaP, treated or not with an inhibitor of RNA Polymerase II (RNAP II), alpha-amanitin. These experiments pointed to a fraction of intronic messages that seems to be insensitive to alpha-amanitin or up-regulated in cells with blocked RNAP II transcription. Keywords: RNA-polymerase II inhibition experiments

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Genome-wide CRISPR loss-of-function screen for α-amanitin

Project description:The “death cap”, Amanita phalloides, is the world’s most poisonous mushroom, responsible for 90% of mushroom-related fatalities. The most fatal component of the death cap is α-amanitin(AMA). Despite its lethal effect, the exact mechanisms of how α-amanitin poisons humans remain unclear, leading to no specific antidote available for treatment. Here, we performed a genome-wide CRISPR loss-of-function screen to identify genes and pathways involved in AMA cytotoxicity.

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The Mechanisms Underlying α-Amanitin Resistance in Drosophila melanogaster: A Microarray Analysis

Project description:The rapid evolution of toxin resistance in animals has important consequences for the ecology of species and our economy. Pesticide resistance in insects has been a subject of intensive study, however, very little is known about how Drosophila species became resistant to natural toxins with ecological relevance, such as α-amanitin that is produced in deadly poisonous mushrooms. Here we performed a microarray study to elucidate the genes, chromosomal loci, molecular functions, biological processes, and cellular components that contribute to the α-amanitin resistance phenotype in Drosophila melanogaster. We suggest that toxin entry blockage through the cuticle, phase I and II detoxification, sequestration in lipid particles, and proteolytic cleavage of α-amanitin contribute in concert to this quantitative trait. We speculate that the resistance to mushroom toxins in Drosophila melanogaster and perhaps in mycophagous Drosophila species has evolved as a cross-resistance to pesticides or other xenobiotic substances.

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RNA half-life analysis after transcriptional blocking with actinomycin D

Project description:Transcriptional profiling of HeLa cells treated with actinomycin D for increasing amounts of time. Relative abundance to control cells was used to estimate the half-life of lncRNAs. Two-condition experiment, actinomycin D-treated vs. untreatted HeLa cells. Biological replicates: 2. Technical replicates: 2.

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BRAF inhibition sensitizes melanoma cells to α-amanitin via decreased RNA polymerase II assembly.

Project description:Despite the great success of small molecule inhibitors in the treatment of patients with BRAFV600E mutated melanoma, the response to these drugs remains transient and patients eventually relapse within a few months, highlighting the need to develop novel combination therapies based on the understanding of the molecular changes induced by BRAFV600E inhibitors. The acute inhibition of oncogenic signaling can rewire entire cellular signaling pathways and thereby create novel cancer cell vulnerabilities. Here, we demonstrate that inhibition of BRAFV600E oncogenic signaling in melanoma cell lines leads to destabilization of the large subunit of RNA polymerase II POLR2A (polymerase RNA II DNA-directed polypeptide A), thereby preventing its binding to the unconventional prefoldin RPB5 interactor (URI1) chaperone complex and the successful assembly of RNA polymerase II holoenzymes. Furthermore, in melanoma cell lines treated with mitogen-activated protein kinase (MAPK) inhibitors, α-amanitin, a specific and irreversible inhibitor of RNA polymerase II, induced massive apoptosis. Pre-treatment of melanoma cell lines with MAPK inhibitors significantly reduced IC50 values to α-amanitin, creating a state of collateral vulnerability similar to POLR2A hemizygous deletions. Thus, the development of melanoma specific α-amanitin antibody-drug conjugates could represent an interesting therapeutic approach for combination therapies with BRAFV600E inhibitors.

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Structural basis of transcription: alpha-amanitin-RNA polymerase II cocrystal at 2.8 A resolution.

Project description:The structure of RNA polymerase II in a complex with the inhibitor alpha-amanitin has been determined by x-ray crystallography. The structure of the complex indicates the likely basis of inhibition and gives unexpected insight into the transcription mechanism.

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The NTCP receptor inhibitor Ezetimibe reduces the toxicity of α-amanitin: in vitro and in vivo study.

Project description:Background and Aims: To verify the protective effect of Ezetimibe, an sodium taurocholate co-transporting polypeptide (NTCP) inhibitor, on α-amanitin poisoning in vitro and in vivo by inhibiting NTCP to prevent α-amanitin into hepatocytes. Approach and Results: In animal experiments, the survival rate was significantly improved in the treatment group. The pathomorphological characteristics of liver and kidney in the treatment group were significantly improved. In cell experiments,The cell viability of the treatment group was significantly improved, and the expression of NTCP in the treatment group was significantly decreased by immunofluorescence. In molecular docking simulations, we demonstrated the potential of NTCP to bind Ezetimibe and α-amanitin, respectively. Transcriptomics in high-throughput sequencing was used to detect the differential metabolic genes between α-amanitin poisoning group and the treatment group, and signal pathway enrichment was used to analyze the significantly different signal pathways. Conclusions: Ezetimibe, as an inhibitor of NTCP, can reduce the entry of α-amanitin into hepatocytes to play a protective role and improve the cell viability and survival rate of mice.

2023-06-30 | GSE235740 | GEO

The response of A549 transcriptome to RNA Pol II slowdown with alpha-amanitin and DRB

Project description:According to current estimates, more than 40% of nascent introns are spliced co-transcriptionally and, consequently, the speed of RNA polymerase II elongation must fundamentally affect the rate of RNA folding, spliceosome assembly, and the resulting mature transcript. RNA-Seq data was generated using RNAPII elongation inhibitors DRB and a-amanitin in A549 cells and used to look at genome-wide splicing changes

2020-06-27 | GSE153303 | GEO

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