Transcriptome profile of Dictyostelium cell during ER-stress
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ABSTRACT:
PROVIDER: PRJNA412540 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6116680.fastq.gz | Fastqsanger.gz | |||
| SRR6116681.fastq.gz | Fastqsanger.gz | |||
| SRR6116682.fastq.gz | Fastqsanger.gz | |||
| SRR6116683.fastq.gz | Fastqsanger.gz | |||
| SRR6116684.fastq.gz | Fastqsanger.gz |
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Project description:The Unfolded Protein Response (UPR) is an adaptive pathway that restores cellular homeostasis after endoplasmic reticulum (ER) stress caused by an impairment of its protein folding capacity. The ER-resident kinase/ribonuclease Ire1 is the only UPR sensor that has been conserved during evolution from yeast to mammals; in these organisms, Ire1 transmits information from the ER to the nucleus trough the non-conventional splicing of Hac1 (yeast)/Xbp1 (metazoans) mRNA. We described the Dictyostelium discoideum ER-stress response and characterized its single bonafide Ire1 orthologue, IreA. We found that tunicamycin (TN) triggers a gene-expression program that increases the protein folding capacity of the ER and that alleviates ER protein load. Further, IreA resulted essential not only for cell-survival after TN-induced ER-stress, but also to accomplish about nearly 40% of the transcriptional changes induced upon a TN treatment. In addition, we described that autophagy is activated in Dictyostelium cells after a TN treatment and that autophagy-defective mutants exhibited increased sensitivity to this drug. The response of Dictyostelium cells to ER-stress involves the combined activation of an IreA-dependent gene expression program and the autophagy pathway.
2018-04-28 | GSE104409 | GEO
Project description:Transcriptional profiling of Control and hac1 deletion mutant in ER stress condition on P. angusta DL1 strain. WT+ER stress vs. hac1 deletion mutant+ER stress. Six-condition experiment: Control+ER stress (TM 30, 60, 120min; DTT 30, 60, 120min) vs. hac1 deletion mutant+ER stress condition (TM 30, 60, 120min; DTT 30, 60, 120min) in P. angusta DL1 strain. Independently grown and harvested. Dye-swapping.
2015-07-22 | E-GEOD-68217 | biostudies-arrayexpress
Project description:Despite the potential of the endoplasmic reticulum (ER) stress response to accommodate adaptive pathways, its integration with other environmental-induced responses is poorly understood in plants. Here, we performed global expression profiling on soybean leaves exposed to polyethylene glycol treatment or to unfolded protein response (UPR) inducers to identify integrated networks between osmotic and ER stress-induced adaptive responses. The results unmasked the major branches of the ER-stress response, which includes enhancing protein folding and degradation in the ER, as well as specific osmotically regulated changes linked to cellular responses induced by dehydration. However, a small proportion (5.5%) of total up-regulated genes represented a shared response that seemed to integrate the two signaling pathways. These co-regulated genes were considered downstream targets based on similar induction kinetics and a synergistic response to the combination of osmotic- and ER-stress-inducing treatments. Genes in this integrated pathway with the strongest synergistic induction encoded proteins with diverse roles. Two of them contained a plant-specific development and cell death (DCD) domain while another had homology to proteins with an ubiquitin-associated (UBA) domain. A NAC domain-containing protein exhibited robust early kinetics of induction consistent with a role as a transfactor. This integrated pathway diverged further from characterized ER-specific branches of UPR as downstream targets were inversely regulated by osmotic stress. Collectively, our results describe a novel branch of the ER stress response that integrates the osmotic signal to potentiate transcription of shared target genes. Keywords: stress response
2007-09-12 | GSE8992 | GEO
Project description:To identify the impact of ER stress on other cellular organelles, cells were treated with ER stress inducer thapsigargin. Transcriptomic profile revealed increased ER stress levels. Deregulated genes was further screened to identify novel ER stress markers of other organelles. Functional charecterization of novel markers were performed to gain insight of the observation.
2025-01-01 | GSE266545 | GEO
Project description:Perturbing ER homeostasis activates stress programs collectively called the unfolded protein response (UPR). The UPR enhances production of ER-resident chaperones and enzymes to reduce the burden of misfolded proteins. Upon resolution of ER stress, excess ER material is removed by ill-defined, selective autophagic programs. Here, using biochemical and cell-based essays, we identify a novel ER-resident autophagy receptor, Sec62, which is activated during recovery from ER stress to selectively deliver ER fragments to the autolysosomal system for clearance. Quantitative mass spectrometry analyses of autolysosomal fractions upon selective inactivation of the Sec62-regulated pathway inform on the selectivity of Sec62-regulated ER-phagy.
2016-10-11 | PXD003961 | Pride
Project description:Endocrine cell ER stress conservation
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Project description:Transcriptome profile of Dictyostelium discoideum slugs in clonal and chimeric development
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Project description:Proteostasis is essential for survival and particularly important for highly specialized post mitotic cells like neurons. Transient reduction of protein synthesis by protein kinase R–like endoplasmic reticulum (ER) kinase (PERK)-mediated phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) is a major proteostatic survival response during ER stress. Paradoxically, neurons are remarkably tolerant to PERK dysfunction, which suggests the existence of cell type-specific mechanisms that secure proteostatic stress resilience. We employed PERK-deficient neuron and astrocyte monocultures to investigate the mechanisms underlying neuron-specific ER stress resilience in the absence of PERK.
2022-06-13 | GSE200742 | GEO
Project description:Purpose: To investigate the critical role ER stress exhibit in cellular crosstalk between tumor cells and macrophages in the tumor microenvironment. We performed the two different polarized macrophages under ER stress and harvested the ER-stressed conditioned media. To figure out how two macrophage polarities generated conditioned media impact LLC tumor cells diversely, we use RNA-sequencing (RNA-seq) strategies to profile the deep-sequencing research and find the potential molecular mechanisms during the ER stress transmission from macrophages to tumor cells. The major differential influences the two macrophages proceeded were attribute to macrophages polarization characteristics, which instruct us to study the two polarized macrophages. Hence, we also performed RNA-sequencing during in vitro stimulation of ER stress inducer Tm in two polarized bone marrow derived macrophages. Methods: After different treatment, LLC tumor cells mRNA was extracted and LLC tumor cells transcriptome profiles were generated by deep sequencing, using Illumina. Under ER stress, the different polarized macrophages transcriptome profiles were also generated by deep sequencing, using Illumina. Results: Macrophages displayed different polarization characteristics could respond to ER stress differentially. Notably, GM-BMDMs were more susceptible to ER stress and facilitated the induction of proinflammatory signals, and M-BMDMs facilitate tumor growth, process, and metastasis. LLC cells exhibit different gene expression profiles in response to transferred ER stress from two polarized macrophage populations. Tumor cells that received transmissible ER stress from M2 macrophages has potential to facilitate the tumor survival, while transmissible ER stress from M1 macrophages could lead to more acute cell death and inflammation. Conclusion: Our study revealed that tumor cells could receive the transmissible ER stress from distinct macrophage populations with different extents of ER stress activation in the tumor microenvironment. The proinflammatory M1-like macrophages respond to ER stress more potently and transmit stronger ER stress to tumor cells. By analyzing the secreted components of two ER stressed macrophage populations, we identified that S100A8 and S100A9, which are dominantly secreted by M1-like macrophages, could lead to significant recipient tumor cell death in synergy with transferred ER stress.
2022-12-22 | GSE193669 | GEO
Project description:Transcriptional profiling of Control and hac1 deletion mutant in ER stress condition on P. angusta DL1 strain.
2015-07-22 | GSE68217 | GEO