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Transcriptome analysis of ire1 mutants after treatment with or without tunicamycin in the presence of actinomycin D

ABSTRACT: Arabidopsis seedlings of wildtype or ire1a ire1b double mutant were treated with or without tunicamycine in the presence of actinomycin D (ActD).

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE39690 | GEO | 2013/03/19

SECONDARY ACCESSION(S): PRJNA171484

REPOSITORIES: GEO

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Transcriptome analysis of ire1 mutants after treatment with or without tunicamycin in the presence of actinomycin D

Project description:Arabidopsis seedlings of wildtype or ire1a ire1b double mutant were treated with or without tunicamycine in the presence of actinomycin D (ActD). 12 samples

2013-03-19 | E-GEOD-39690 | biostudies-arrayexpress

ire1 double mutant vs wild-type in response to tunicamycin

Project description:Arabidopsis thaliana wild-type and ire1a/ire1b double mutant plants were treated with tunicamycin. RNA was extracted and subjected to microarray analysis.

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RNA-seq of Arabidopsis thaliana shoots and roots treated with tunicamycin: a comparison between double mutant (ire1a ire1b) and wild type genotypes.

Project description:The aim of this study is to identify genes whose expression is under the control of IRE1A and IRE1B during a chronic proteotoxic endoplasmic reticulum stress induced by tunicamycin. The transcriptional response has been measured in separated shoot and root tissues from Arabidopsis seedlings.

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Actinomycin targets NPM1c-primed mitochondria in AML

Project description:Acute myeloid leukemia (AML) pathogenesis often involves a mutation in the NPM1 nucleolar chaperone, but the bases for its transforming properties and association with favorable outcome remain incompletely understood. Here we demonstrate that an oncogenic mutant form of NPM1 (NPM1c) hampers formation of PML nuclear bodies (NBs), key senescence effectors, and impairs mitochondrial function to drive an integrated stress response. Actinomycin D (ActD), an antibiotic with unambiguous clinical efficacy in relapsed/refractory NPM1c-AMLs, preferentially targets these primed mitochondria, activating cGAS signaling and boosting ROS production. The later restores PML NB formation to drive senescence of NPM1c-AMLs cells. Dual targeting of mitochondria by Venetoclax and ActD synergized for AML elimination. Our studies reveal a central role of mitochondria downstream of NPM1c and implicate a mitochondrial/ROS/PML/TP53 senescence pathway as a key effector of ActD-based, and possibly others, chemotherapies.

2021-12-17 | PXD025507 | Pride

Transcription profiling of yeast using samples prepared with actinomycin D to exclude antisense artifacts

Project description:Recent transcription profiling studies have revealed an unanticipatedly large proportion of antisense transcription across eukaryotic and bacterial genomes. However, the extent and significance of antisense transcripts is controversial partly because experimental artifacts are suspected. Here, we present a method to generate clean genome-wide transcriptome profiles, using actinomycin D (ActD) during reverse transcription. We show that antisense artifacts appear to be triggered by spurious synthesis of second-strand cDNA during reverse transcription reactions. Strand-specific hybridization signals obtained from Saccharomyces cerevisiae tiling arrays were compared between samples prepared with and without ActD. Use of ActD removed about half of the detectable antisense transcripts, consistent with their being artifacts, while sense expression levels and about 200 antisense transcripts were not affected. Our findings thus facilitate a more accurate assessment of the extent and position of antisense transcription, towards a better understanding of its role in cells.

2007-10-30 | E-TABM-361 | biostudies-arrayexpress

IRE1 inhibitor [RNA-seq]

Project description:The role of the unfolded protein response (UPR) in the cellular innate response to RSV infection is not fully understood. To better the genomic targets for the IRE1-XBP1 pathway, RNA seq was conducted on RSV-infected small airway cells in the absence or presence of RSV infection and in the absence or presence of a selective IRE1a RNAse inhibitor. We identified expression changes in ~3.2K genes; of these, 279 required IRE1 and were enriched in IL-10 signaling and cytokine signaling pathways. These data indicate that IRE1a-XBP1s regulates genes important in epithelial mesenchymal transition, hexosamine biosynthesis and anti-viral signaling.

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Proteasome inhibition sensitizes anaplastic Wilms tumor to actinomycin D

Project description:Wilms tumor is the most common kidney cancer in children, and anaplastic Wilms tumor is the most chemoresistant histological subtype. Here we explore how anaplastic Wilms tumor cells evade the common chemotherapeutic drug actinomycin D, which inhibits ribosomal biogenesis. We found that, when ribosomal capacity is limited by actinomycin D treatment, anaplastic Wilms tumor cells preferentially translate proteasome components and upregulate proteasome activity. Accordingly, increased proteasome levels are associated with anaplastic histology and with worse prognosis in Wilms tumor. Lastly, we show that the proteasome inhibitor bortezomib sensitizes cells to actinomycin D treatment both in vitro and in vivo.

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The mRNA decay analysis of Plasmodium falciparum parasites with disrupted PfNot1.1 (PF3D7_1103800) at 24 hour post-invasion.

Project description:The study aims to investigate functions of PfNOT1.1 in regulating mRNA decay in the malaria parasite, P. falciparum. To achieve this goal, transcription was blocked by actinomycin D (actD) and the transcriptional profilling of parasites was analyzed by microarray technology.

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Low-dose actinomycin D preferentially disrupts EWS-FLI1DNA binding.

Project description:Fusion of the EWS gene to FLI1 produces a fusion oncoprotein that drives an aberrant gene expression program responsible for the development of Ewing sarcoma. We used a homogenous proximity assay to screen for compounds that disrupt the binding of EWS-FLI1 to its cognate DNA targets. A number of DNA-binding chemotherapeutic agents were found to non-specifically disrupt protein binding to DNA. In contrast, actinomycin D was found to preferentially disrupt EWS-FLI1 binding by comparison to p53 binding to their respective cognate DNA targets in vitro. In cell-based assays, low concentrations of actinomycin preferentially blocked EWS-FLI1 binding to chromatin, and disrupted EWS-FLI1-mediated gene expression. Higher concentrations of actinomycin globally repressed transcription. These results demonstrate that actinomycin preferentially disrupts EWS-FLI1 binding to DNA at selected concentrations. Although the window between this preferential effect and global suppression is too narrow to exploit in a therapeutic manner, these results suggest that base-preferences may be exploited to find DNA-binding compounds that preferentially disrupt subclasses of transcription factors.

2013-08-26 | GSE45414 | GEO

Exploring the link between ER stress and autophagy in Arabidopsis

Project description:Autophagy is a conserved process in eukaryotes that contributes to cell survival in response to stress. Previously, we found that ER stress induces autophagy in a manner dependent upon IRE1b, an ER membrane-associated factor involved in the splicing of bZIP60 mRNA. IRE1 is a dual protein kinase and ribonuclease, and here we studied the involvement of the protein kinase catalytic domain, nucleotide binding and RNase domains of IRE1b in activating autophagy. Autophagy was assessed by quantifying the numbers of autophagosomes in transgenic Arabidopsis seedlings bearing mutations in the various IRE1b domains. The results showed that nucleotide binding and RNase activity of IRE1b are required for ER stress-mediated autophagy. The RNase activity is involved in IRE1b’s mRNA splicing function, but its principal splicing target, bZIP60, is not involved in IRE1b’s activation of autophagy. We therefore considered other roles for IRE1b in the activation of autophagy. Clustering of ER localized IRE1b-YFP was observed when seedlings were subjected to ER stress, and so we investigated whether IRE1b clustering induced autophagy. However, the RNase knockout mutation in IRE1b still undergoes clustering, suggesting that IRE1b clustering does not induce autophagy. In response to ER stress, the RNase of IRE1 has been found to engage in another activity called Regulated Ire1-Dependent Decay of Messenger RNA (RIDD), which is the promiscuous degradation of other mRNA in response to ER stress. By analyzing the RNA-seq data, 12 RIDD target genes were picked up for testing their role in inhibiting autophagy, and glucosidase 21 and peroxidase 14 are proved to be degraded to support the induction of autophagy by ER stress.

2018-03-31 | GSE99576 | GEO

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