Cellular response to heat shock and ER stress
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE65636 | GEO | 2015/09/04
SECONDARY ACCESSION(S): PRJNA274568
REPOSITORIES: GEO
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Project description:Analysis of the coordinated transcriptional reponse to heat shock and ER stress mRNA profiles of NIH3T3 cells which stably expressing DD-sfGFP were generated by deep sequencing, in triplicate, using Illumina HiSeq. The samples were collected from indicated timepoints after exposed to either heat stress or ER stress.
2015-09-04 | E-GEOD-65636 | biostudies-arrayexpress
Project description:We examined the stress response in Entamoeba histolytica trophozoites by comparing untreated log-phase HM-1:IMSS trophozoites to those subjected to heat shock at 42C for 1 hour. Keywords: stress reponse We compared two arrays from normal trophozoites to two arrays from trophozoites subjected to heat shock.
2007-03-01 | E-GEOD-6650 | biostudies-arrayexpress
Project description:We examined the stress response in Entamoeba histolytica trophozoites by comparing untreated log-phase HM-1:IMSS trophozoites to those subjected to heat shock at 42C for 1 hour. Keywords: stress reponse
2007-03-01 | GSE6650 | GEO
Project description:We investigated the root growth of several knockout mutants of heat shock protein family genes and found that heat stress response was compromised in these mutants compared to wild type plants. It suggested that heat shock protein genes including heat shock protein genes including HSP17s, HSP23s, HSP101, and HSFA2 proteins are deployed upon exposure to Cs for plant stress tolerance. Our study provided novel insights into the molecular events occurring in Cs-stressed plants.
2024-04-06 | GSE262902 | GEO
Project description:Whole-genome analysis of heat shock factor binding sites in Drosophila melanogaster. Heat shock factor IP DNA or Mock IP DNA from heat shocked Kc 167 cells compared to whole cell extract on Agilent 2x244k tiling arrays.
2011-01-05 | GSE19744 | GEO
Project description:Heat shock response (HSR) is a cellular defense mechanism against various stresses. Both heat shock and proteasome inhibitor MG132 cause the induction of heat shock proteins, a distinct feature of HSR. To better understand the molecular basis of HSR, we subjected the mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant, TR-RIF-1 cells, to heat shock and MG132. We compared mRNA expressions using microarray analysis during recovery after heat shock and MG132 treatment. This study led us to group the 3,245 up-regulated genes by heat shock and MG132 into three families: genes regulated 1) by both heat shock and MG132 (e.g. chaperones); 2) by heat shock (e.g. DNA-binding proteins including histones); and 3) by MG132 (e.g. innate immunity and defense-related molecules).
2011-11-09 | GSE24197 | GEO
Project description:Cells respond to many different types of stresses by overhauling gene expression patterns, both at the transcriptional and translational level. Under heat stress, global transcription and translation are inhibited, while the expression of chaperone proteins are preferentially favored. As the direct link between mRNA transcription and protein translation, tRNA expression is intricately regulated during the stress response. Despite extensive research into the heat shock response (HSR), the regulation of tRNA expression by RNA Polymerase III (Pol III) transcription has yet to be fully elucidated in mammalian cells. Here, we examine the regulation of Pol III transcription during different stages of heat shock stress in mouse embryonic stem cells (mESCs). We observe that global transcription of tRNAs is downregulated after 30 minutes of heat shock, followed by an overall increase in tRNA transcription after 60 minutes of heat shock. This effect is more evident in tRNAs, though other RNA Pol III gene targets are also similarly affected. Notably, we show that the down-regulation at 30 minutes of heat shock is independent of HSF1, the master transcription factor of the HSR, but that the subsequent increase in expression at 60 minutes requires HSF1. Taken together, these results demonstrate an adaptive RNA Pol III response to heat stress, and an intricate relationship between the canonical HSR and tRNA expression.
2025-03-04 | GSE282678 | GEO
Project description:Post-embryonic plant development must be coordinated in response to and with environmental feedback. Development of above-ground organs is orchestrated from stem cells in the center of the shoot apical meristem (SAM). Heat can pose significant abiotic stress to plants and induce a rapid heat shock response, developmental alterations, chromatin decondensation, and activation of transposable elements (TEs). However, most plant heat-stress studies are conducted with seedlings, and we know very little about cell-type-specific responses. Here we use fluorescent-activated nuclear sorting to isolate and characterize stem cells of wild type and mutants defective in TE defense and chromatin compaction after heat shock and after a long recovery. Our results indicate that stem cells can suppress heat shock response pathways to maintain developmental programs. Furthermore, mutants defective in DNA methylation fail to recover efficiently from heat stress and persistently activate heat shock factors and heat-inducible TEs. Heat stress also induces DNA methylation epimutations, especially in the CHG context, and we find hundreds of DNA methylation changes three weeks after stress. Our results underline the importance of disentangling cell type-specific environmental responses for understanding plant development.
2023-09-30 | GSE223914 | GEO
Project description:Post-embryonic plant development must be coordinated in response to and with environmental feedback. Development of above-ground organs is orchestrated from stem cells in the center of the shoot apical meristem (SAM). Heat can pose significant abiotic stress to plants and induce a rapid heat shock response, developmental alterations, chromatin decondensation, and activation of transposable elements (TEs). However, most plant heat-stress studies are conducted with seedlings, and we know very little about cell-type-specific responses. Here we use fluorescent-activated nuclear sorting to isolate and characterize stem cells of wild type and mutants defective in TE defense and chromatin compaction after heat shock and after a long recovery. Our results indicate that stem cells can suppress heat shock response pathways to maintain developmental programs. Furthermore, mutants defective in DNA methylation fail to recover efficiently from heat stress and persistently activate heat shock factors and heat-inducible TEs. Heat stress also induces DNA methylation epimutations, especially in the CHG context, and we find hundreds of DNA methylation changes three weeks after stress. Our results underline the importance of disentangling cell type-specific environmental responses for understanding plant development.
2023-09-30 | GSE223850 | GEO
Project description:Stress response pathways allow cells to rapidly sense and respond to deleterious environmental changes, including those caused by pathophysiological disease states. A previous screen for small molecules capable of activating the human heat shock response identified the triterpenoid celastrol as a potent activator of the heat shock transcription factor HSF1. We show here that celastrol likewise activates the homologous Hsf1 of Saccharomyces cerevisiae. Celastrol induced Hsf1 hyperphosphorylation and concurrently activated a synthetic transcriptional reporter as well as endogenous inducible Hsp70 proteins at the same effective concentration seen in mammalian cells. Moreover, celastrol treatment conferred significant resistance to subsequent lethal heat shock. Transcriptional profiling experiments revealed that in addition to Hsf1, celastrol treatment induced the Yap1-dependent oxidant defense regulon. Oxidative stress-responsive genes were likewise induced in mammalian cells, demonstrating that celastrol simultaneously activates two major cellular stress-mediating pathways. As the induction of cellular stress pathways has implications in the treatment of a variety of human diseases including neurodegenerative diosorders, cardiovascular disease and cancer, celastrol thus represents an attractive therapeutic compound. Keywords: single-dose, single time-point gene induction by natural small molecule celastrol compared to heat shock in wild type (BY4741) Saccahromyces cerevisiae
2006-08-26 | GSE5608 | GEO