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Expression dynamics in mammalian cells responding to protein misfolding stress

ABSTRACT: We have employed whole genome microarray expression profiling to track the transcriptome expression change under DTT induced protein misfolding stress. The relative importance of gene expression regulation at the mRNA versus the protein-level is a matter of ongoing debate. We present an in-depth analysis of a cervical cancer cell line responding to protein misfolding stress induced by dithiothreitol treatment, quantifying the dynamics of mRNA and protein concentrations for >3,500 genes over a time-course 30 hours. While the early phase of the experiment (

ORGANISM(S): Homo sapiens

PROVIDER: GSE67901 | GEO | 2015/08/15

SECONDARY ACCESSION(S): PRJNA281173

REPOSITORIES: GEO

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Expression dynamics in mammalian cells responding to protein misfolding stress

Project description:The relative importance of gene expression regulation at the mRNA versus the protein-level is a matter of ongoing debate. We present an in-depth analysis of a cervical cancer cell line responding to protein misfolding stress induced by dithiothreitol treatment, quantifying the dynamics of mRNA and protein concentrations for >3,500 genes over a time-course 30 hours. While the early phase of the experiment (<two hours) was marked by apoptosis, surviving cells were marked by a strong response to unfolded proteins and stress of the endoplasmatic reticulum, specifically during the intermediate phase (two to eight hours). Using statistical time series analysis, we detected significant changes in the regulatory parameters at the RNA-level, caused by transcription and mRNA degradation, and at the protein-level, caused by translation and protein degradation. mRNA- and protein-level regulation were of equal importance (XX and YYY%, respectively), but displayed different magnitudes and dynamics: mRNA fold changes were much smaller on average than those of the proteins. While our method did not capture immediate changes, we found the strongest regulatory response between two and eight hours after the treatment. mRNA-level regulation showed a spike around this time interval, while protein-level regulation was delayed and continued at slower pace until the end of the experiment.

2016-03-14 | PXD002039 | Pride

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Mapping multi-layered regulation in response to environmental stress

Project description:We have mapped transcript and protein concentrations in cervical cancer cells responding to treatment with tunicamycin over an eight hour time course. We complement this dataset with RNA footprints of ribosomes and non-ribosomal proteins to determine changes in translation and trans-factor binding. The goals of this study are to unveil the time dependent complexity of the signaling pathways at the level of transcription and translation during different stress conditions like stress of the endoplasmic reticulum and oxidative stress.

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Project description:Expression dynamics in mammalian cells responding to protein misfolding stress

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DELE1 mitochondrial integrated stress response to CHCHD10 G58R protein misfolding in striated muscle [RNA-seq]

Project description:Transcriptional mitochondrial stress response to CHCHD10 G58R protein misfolding in mouse heart, gastrocnemius, and tibalis anterior muscle the presence and absence of the DELE1 mitochondrial integrated stress responses

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Redox control of the cAMP/PKA pathway during protein misfolding stress

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QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis [RNA-seq]

Project description:Perturbation of tissue homeostasis accompanies a diversity of inflammatory pathologies and imposes metabolic constraints at the cellular level that elicit ER stress, protein misfolding, and cell death. In response to ER stress, cells initiate the unfolded protein response (UPR), which determines divergent cell fate decisions, either promoting recovery of ER proteostasis and cell survival or triggering programmed cell death. However, the mechanisms by which the UPR transitions from the adaptive to terminal state are not fully understood. Here, we identify QRICH1 as a previously uncharacterized transcriptional regulator of a gene modulethat differentially engages the terminal versus adaptive UPR.

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QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis [ChIP-seq]

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Temporal scRNAseq identifies dynamic transcriptional programs that dictate the outcome of ER stress

Project description:Perturbation of tissue homeostasis accompanies a diversity of inflammatory pathologies and imposes metabolic constraints at the cellular level that elicit ER stress, protein misfolding, and cell death. In response to ER stress, cells initiate the unfolded protein response (UPR), which determines divergent cell fate decisions, either promoting recovery of ER proteostasis and cell survival or triggering programmed cell death. However, the mechanisms by which the UPR transitions from the adaptive to terminal state are not fully understood. Here, we leverage single-cell genomics to define dynamic transcriptional states associated with the adaptive versus terminal UPR in the intestinal epithelium. We recovered the terminal-UPR signature, which dictates adaptation versus programmed cell death in response to ER stress.

2021-02-17 | GSE149633 | GEO

INS1-EGFP-L10a stable cell lines treated with Thapsigargin

Project description:INS1-EGFP-L10a stable cell lines were induced with Doxycycline (Dox) for 24 hours, then either untreated or treated for 30 minutes with 1uM Thapsigargin to induce ER stress. Total RNA was purified with Trizol, and RIP RNA samples were extracted by immunoaffinity purification using an EGFP antibody We aimed to determine which genes are enriched under ER stress at the polyribosomal level. To do this we compared expression profiles of Total RNA with and without ER stress, and Immunoaffinity purified RNA (RIP) with and without ER stress. Microarray results of INS-1 EGFP-L10a cells either untreated or treated with 1uM Thapsigargin (Tg) in triplicate. Both Total RNA and RNA isolated from ribosomal Immunoprecipitation (RIP) When unfolded proteins accumulate to irremediably high levels within the endoplasmic reticulum (ER), intracellular signaling pathways called the unfolded protein response (UPR) become hyperactivated to cause programmed cell death. We discovered that thioredoxin-interacting protein (TXNIP) is a critical node in this “Terminal UPR”. TXNIP becomes rapidly induced by hyperactivated IRE1a, an ER bifunctional kinase/endoribonuclease (RNase). IRE1a controls TXNIP mRNA stability by reducing levels of a TXNIP destabilizing micro-RNA, miR-17. In turn, elevated TXNIP protein activates the NLRP3 inflammasome, causing Caspase-1 cleavage and interleukin 1b (IL-1b) secretion. Txnip gene deletion reduces pancreatic b-cell death during ER stress, and suppresses diabetes caused by proinsulin misfolding in the Akita mouse. Finally, small molecule IRE1a RNase inhibitors suppress TXNIP production to block IL-1b secretion. In summary, the IRE1a-TXNIP pathway is used in the terminal UPR to promote sterile inflammation and programmed cell death, and may be targeted to develop new treatments for degenerative diseases driven by ER stress.

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