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Persistent ER stress in maize seedlings engages ZmIRE1 in a multiphasic process that transitions from prosurvival activities to cell death [RNA-Seq]

ABSTRACT: We tracked the gene expression events following treatment of maize seedlings with the endoplasmic reticulum (ER) stress agent tunicamycin. ER stress elicits the unfolded protein response (UPR) and when plants are faced with persistent stress, the UPR transitions from an adaptive or cell survival phase to programmed cell death.

ORGANISM(S): Zea mays

PROVIDER: GSE111250 | GEO | 2018/05/30

REPOSITORIES: GEO

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Persistent ER stress in maize seedlings engages ZmIRE1 in a multiphasic process that transitions from prosurvival activities to cell death [ATAC-Seq]

Project description:Nucleus was isolated from flash frozen from tunicamycin treated (0,6 and 12 hours) maize root samples, purified, then transposition reaction and and purification steps were carried out following the standard ATAC-seq protocol

2018-05-30 | GSE110987 | GEO

Nuclear receptor LRH-1/NR5A2 is required and targetable for liver endoplasmic reticulum stress resolution.

Project description:Chronic endoplasmic reticulum (ER) stress results in toxicity that contributes to multiple human disorders. We report a stress resolution pathway initiated by the nuclear receptor LRH-1 that is independent of known unfolded protein response (UPR) pathways. Like mice lacking primary UPR components, hepatic Lrh-1-null mice cannot resolve ER stress, despite a functional UPR. In response to ER stress, LRH-1 induces expression of the kinase Plk3, which phosphorylates and activates the transcription factor ATF2. Plk3-null mice also cannot resolve ER stress, and restoring Plk3 expression in Lrh-1-null cells rescues ER stress resolution. Reduced or heightened ATF2 activity also sensitizes or desensitizes cells to ER stress, respectively. LRH-1 agonist treatment increases ER stress resistance and decreases cell death. We conclude that LRH-1 initiates a novel pathway of ER stress resolution that is independent of the UPR, yet equivalently required. Targeting LRH-1 may be beneficial in human disorders associated with chronic ER stress. 24 total samples. One sample represents one mouse. Three samples were analyzed from the following groups: Lrh-1 f/f (control littermates) treated with vehicle, Lrh-1 f/f treated with tunicamycin (TM; 1mg/kg BW for 24h), Lrh-1 f/f treated with tunicamycin and DLPC (100mg/kg BW 4x), Lrh-1 f/f treated with tunicamycin and vehicle for DLPC, Lrh-1 liver-specific KO mice (LKO) treated with vehicle, Lrh-1 LKO treated with tunicamycin, and Lrh-1 LKO treated with tunicamycin and DLPC, Lrh-1 LKO treated with tunicamycin and vehicle for DLPC

2015-05-12 | E-GEOD-68718 | biostudies-arrayexpress

SILAC-based quantitative proteomics of endoplasmic reticulum stress

Project description:ER stress and the unfolded protein response (UPR) involve extensive proteome remodeling in many cell compartments. However, a comprehensive analysis has been lagging due to technological limitations. Here we employ SILAC-based proteomics to quantify over 6,200 proteins at increasing concentrations of tunicamycin in HeLa cells. We further compare the effects of tunicamycin to those of thapsigargin and DTT, both activating the UPR through different mechanisms. The systematic description of the proteome-wide expression changes following proteostatic stress is a resource for the scientific community, which enables to discover novel players involved the pathophysiology of disorders linked to proteostasis. Here, we identified 38 proteins, not previously linked to the UPR, whose expression increases, of which 15 would likely remediate ER stress, and the remainder may contribute to pathological outcomes. Unexpectedly, we see few strongly downregulated proteins, despite expression of the pro-apoptotic transcription factor CHOP, suggesting that IRE1-dependent mRNA decay (RIDD) has a limited contribution to ER-stress mediated cell death in our system.

2019-11-01 | PXD013496 | Pride

Ribosomal protein S7 ubiquitination during ER stress in yeast is associated with selective mRNA translation and stress outcome.

Project description:eIF2α phosphorylation-mediated translational regulation is crucial for global translation repression by various stresses, including the unfolded protein response (UPR). However, translational control during UPR has not been demonstrated in yeast. This study investigated ribosome ubiquitination-mediated translational controls during UPR. Tunicamycin-induced ER stress enhanced the levels of ubiquitination of the ribosomal proteins uS10, uS3 and eS7. Not4-mediated monoubiquitination of eS7A was required for resistance to tunicamycin, whereas E3 ligase Hel2-mediated ubiquitination of uS10 was not. Ribosome profiling showed that the monoubiquitination of eS7A was crucial for translational regulation, including the upregulation of the spliced form of HAC1 (HAC1i) mRNA and the downregulation of Histidine triad NucleoTide-binding 1 (HNT1) mRNA. Downregulation of the deubiquitinating enzyme complex Upb3-Bre5 increased the levels of ubiquitinated eS7A during UPR in an Ire1-independent manner. These findings suggest that the monoubiquitination of ribosomal protein eS7A plays a crucial role in translational controls during the ER stress response in yeast.

2020-11-12 | GSE128578 | GEO

Secretome characterization of nucleus pulposus (NP) cells subjected to ER stress

Project description:Objective: Induction of ER stress has been shown to promote NP cell apoptosis and disc degeneration. However, little is known about its regulation by hypoxia and its contribution to extracellular matrix homeostasis. Methods: NP cells were culture under hypoxia (1% O2) and normoxia (21% O2) to assess ER stress status. Tunicamycin and thapsigargin were used to induce canonical ER stress pathways and effects on cell secretome were assessed by proteomic analysis using mass spectrometry. The relevance of these findings to aging and degeneration was investigated by analyzing microarray data of NP tissues from aged mice (GSE134955) and degenerated human discs (GSE70362). Results: NP cells exhibited lower ER stress levels under hypoxia. ER stress inducers tunicamycin and thapsigargin promoted a canonical unfolded protein response. UPR further induced HIF-1 activity under hypoxia. NP cell secretome under ER stress showed an increased secretory pathway with a concomitant decrease in collagens, HAPLN1, and cell adhesion related proteins. Similar to our cell culture studies, NP tissues from aged mice and degenerated human discs presented higher levels of UPR markers and decreased levels of matrix components.

2020-12-03 | PXD019151 | Pride

Effect of Tunicamycin on Bovine Capillary Endothelial Cells

Project description:GPT inhibitor Tunicamycin develops ER stress causing anti-angiogenic response in breast tumor microvasculature due to unfolded protein response-mediated apoptosis. cDNA microarray identified 123 and 454 differentially regulated genes with 10 genes overlapping between 3h and 32 h of Tunicamycin treatment. Alg-2 expression is inconsistent but not the Dpms. Evidences support that Tunicamycin completely destroys DPMS activity in capillary endothelial cells without affecting its protein or the mRNA levels but by knocking down the phosphorylation. DPMS’ contribution to developing upr during ER stress has therefore been evaluated because of its inherent regulatory property of GPT. FTIR spectroscopy confirmed protein denaturation. Restablishing the phosphorylation status helps the DPMS regaining its activity. As a result, ER stress is reduced reversing apoptosis and bringing more cells into cycling with normal cellular morphology. Furthermore, differential expression of DPMS in breast tumor microvasculature during Tunicamycin therapy raises its potential as a tumor prognostic marker in the clinic.

2017-11-15 | GSE33729 | GEO

Persistent ER stress in maize seedlings engages ZmIRE1 in a multiphasic process that transitions from prosurvival activities to cell death

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-05-30 | GSE111251 | GEO

RNA-seq of WT vs isw1 delta S. cerevisiae cells during Unfolded Protein Response time course

Project description:UPR Time course of WT and isw1delta cells. ER stress induced by 1ug/mL Tunicamycin treatment. 3 time points: Untreated, Tm 2H , Wash 3H Untreated = no treatment T2 = two-hour Tm treatment (1ug/mL) T3= Wash 3H = wash of the cells after the two-hour Tm treatment and 3-hour recovery in medium without drug

2022-10-06 | E-MTAB-10511 | biostudies-arrayexpress

Transcription profiling of human cancer cells treated with unfolded protein response modulators under endoplasmic reticulum stress conditions

Project description:The unfolded protein response (UPR) is a cellular defense mechanism against glucose deprivation, a cell condition that occurs in solid tumors. A key feature of the UPR is the activation of the transcription program that allows the cell to cope with endoplasmic reticulum (ER) stress. We used micoarrays to show that the UPR transcription program is disrupted by the antitumor macrocyclic compound versipelostatin (VST) and antidiabetic biguanides metformin, buformin and phenformin, depending on cellular glucose availability. Experiment Overall Design: Total 42 samples were prepared for RNA extraction and hybridization on Affymetrix microarrays. Experiment Overall Design: To induce the UPR, we treated cells (HeLa, HT-29, HT1080, MKN74) for 15 or 18 hours under ER stress conditions by replacing the medium with glucose-free medium or by adding either 2-Deoxy-D-glucose (2DG) or Tunicamycin (TM) to glucose-containing medium. UPR modulators (VST, biguanides or pyrvinium pamoate) were added at various final concentrations immediately after cells were placed in glucose-free medium or just before the chemical stressors were added to glucose-containing culture medium.

2009-06-01 | E-GEOD-13548 | biostudies-arrayexpress

Analysis of gene expression changes induced in wild-type or Atf6a-/- mice by treatment with tunicamycin for 34h

Project description:Protein misfolding stress in the endoplasmic reticulum (ER) leads to dysregulation of lipid metabolism in the liver, and ER stress is associated with human diseases that are accompanied by hepatic lipid accumulation, including obesity, alcoholism, and viral hepatitis; yet the pathways leading from ER stress to the regulation of lipid metabolism are poorly understood. Working exclusively in vivo, we used a “bottom-up” approach to infer pathways in the genetic regulation of lipid metabolism by the UPR. We used a functional genomics to link gene expression patterns taken from microarray data to the severity and persistence of ER stress, using mice lacking the UPR signaling molecule ATF6α. This approach revealed that functionally related genes clustered into a small number of distinct expression profiles, and that lipid oxidation and efflux were targets for coordinated transcriptional suppression during ER stress.Our results establish a framework for hepatic gene regulation during ER stress. Atf6a-/- or +/+ mice of variable age and gender were injected intraperitoneally with 1 mg/kg tunicamycin or vehicle. 3 separate mice were used in each group. 34h after injection, mice were sacrificed and total RNA was prepared from resected livers.

2013-09-04 | E-GEOD-48935 | biostudies-arrayexpress

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