Short heat shock has a long-term effect on mesenchymal stem cells’ transcriptome
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ABSTRACT:
ORGANISM(S): Bos taurus
PROVIDER: GSE214467 | GEO | 2023/07/21
REPOSITORIES: GEO
Similar Datasets
Project description:Ambient temperature is one of the most important environment factors that direct all organisms for morphogenesis, metabolisms and growth. Plants have evolved efficient mechanisms adapting temperature fluctuation such as heat stress response (HSR). Although transcriptional regulatory network of plant HSR has been established, little is known on the genome-wide transcriptional changes within first several minutes upon heat shock (HS). To precisely measure the very first wave of transcriptional response to HS, we investigated the nascent RNA and mature mRNA from plant leaf tissue exposure to 5-min HS treatment using global run-on sequencing (GRO-seq) and RNA sequencing (RNA-seq) methods. We found that only a small group of genes were both up- or down-regulated at nascent RNA and mRNA levels. Primed plants that already exposed to a mild heat stress induced a more drastic transcriptomic alteration than naïve plants which had not experienced a heat stress. Group A1 HEAT SHOCK TRANSCRIPTION FACTORs (HsfA1s) are the major transcription factors in charge of the very early transcriptional HSR. Within 5-minute HS, we also observed that: 1) Engaged RNA polymerase II (Pol II) was accumulated downstream of transcription start sites; 2) 5' pause-release is a rate limiting step for induction of some heat shock protein genes; 3) A good number of genes switched transcription modes; 4) Pervasive read-through was induced at terminators. Plants' HSR is transcriptionally very quick. GRO-seq is sensitive and robust to detect quick response to HS. Heat stress memory takes place at multiple steps of transcription cycles such as Pol II recruitment, 5' pausing, elongation and termination.
2020-07-11 | GSE128698 | GEO
Project description:Time-resolved proteomic profiling of SGs from cultured human U2OS cells over a prolonged heat-shock (HS) and a successive recovery period, sampling at the 6 time points of HS exposure (10, 20, 30, 60, 120, 180 min), as well as 2 time points of recovery (5, 10 min). From the sampled cells, we prepared SG samples using a differential centrifugation plus endogenous G3BP1 immunoprecipitation protocol. Peptides were subsequently TMT-labeled and analyzed by quantitative LC-MS/MS. In G3BP1 dataset, rep1-rep3, HS-10, 20, 30, 60, 120, 180, re5, re10, SG-ls, G3BP1-IP samples were labeled with TMT-126, 127N, 127C, 128N, 128C,129N, 129C, 130N, 130C, 131 label Reagents, respectively; G3BP1_HS0 was a dataset created to integrate a non-heat shock control (HS-0) into the G3BP1 dataset, contains HS0, HS10, and HS60, and the results was integrated into the G3BP1 dataset using the ComBat processing, HS-0_rep1, HS-0_rep2, HS-0_rep3, HS-10_rep1, HS-10_rep2, HS-10_rep3, HS-60_rep1, HS-60_rep2, HS-60_rep3 samples were labeled with TMT-126, 127N, 127C, 128N, 128C,129N, 129C, 130N, 130C label Reagents, respectively. In CAPRIN1 dataset, rep1-rep3, HS-0, 10, 20, 30, 60, 120, 180, re5, re10 samples were labeled with TMT-126, 127N, 127C, 128N, 128C,129N, 129C, 130N, 130C label Reagents, respectively.
2023-08-30 | MSV000092790 | MassIVE
Project description:Plants and animals share similar mechanisms in the heat-shock (HS) response, such as synthesis of the conserved HS proteins (Hsps). However, because plants are confined to a growing environment, in general they require unique features to cope with heat stress. We have analyzed the function of a novel Hsp, heat-stress-associated 32-kD protein (Hsa32), which is highly conserved in land plants but absent in most other organisms. The gene responds to HS at the transcriptional level in moss, Arabidopsis, and rice. Like other Hsps, Hsa32 protein accumulates greatly in Arabidopsis seedlings after HS treatment. Disruption of Hsa32 by T-DNA insertion does not affect growth and development under normal conditions. However, the acquired thermotolerance in the knockout line was compromised following a long recovery period (> 24 h) after an acclimation HS treatment, when a severe HS challenge killed the mutant but not the wild-type plants, but no significant difference was observed if they were challenged within a short recovery period. Microarray analysis of the knockout mutant indicates that only the expression of Hsa32 was significantly altered in HS response. Taken together, our results suggest that Hsa32 is not required for the induction but maintenance of acquired thermotolerance. This report provides direct evidence that a plant-specific Hsp plays an important role in thermotolerance. Keywords: heat shock response
2006-03-20 | GSE4062 | GEO
Project description:JN54 (wild-type) cells were incubated in YPD medium at 30 degrees C to a logarithmic phase (OD660=1), followed by treatment with mild heat-shock at 43 degrees C for 30 min in pre-warmed (43 degrees C) 100ml of YPD medium using 500 ml Erlenmeyer flask. JN54 (wild-type) cells were incubated in YPD medium at 30 degrees C to a logarithmic phase (OD660=1), followed by treatment with mild heat-shock at 43 degrees C for 60 min in pre-warmed (43 degrees C) 100ml of YPD medium using 500 ml Erlenmeyer flask. Keywords: Stress response
2005-09-21 | GSE3316 | GEO
Project description:Analysis of embryos exposed to either: [1] 40 uM 4-hydroperoxycyclophosphamide for 1 or 5 hours at 37°C [2] 43°C heat shock for 15 minutes followed by 1 or 5 hours at 37°C This SuperSeries is composed of the following subset Series: GSE866: CP 1hr GSE869: HS 1hr GSE870: HS 5hr GSE888: CP 5hr
2004-02-23 | E-GEOD-905 | biostudies-arrayexpress
Project description:Heat shock (HS) causes dramatic and rapid changes in transcription of thousands of genes in metazoans. We have used insitu Hi-C in Drosophila S2 and human K562 cells to determine the effects of HS upon chromatin conformation. Our study shows that topologically associated domains (TADs), compartments and distal regulatory interactions remain unchanged upon HS.
2019-06-07 | GSE130776 | GEO
Project description:Heat shock (HS) causes dramatic and rapid changes in transcription of thousands of genes in metazoans. We have used insitu Hi-C in Drosophila S2 and human K562 cells to determine the effects of HS upon chromatin conformation. Our study shows that topologically associated domains (TADs), compartments and distal regulatory interactions remain unchanged upon HS.
2019-06-07 | GSE130758 | GEO
Project description:Periodic fever is the most characteristic clinical feature of human malaria. However, how parasites survive malarial febrile episodes, which often involve temperatures of >40ºC, is not known. Plasmodium falciparum cultures adapted to periodic heat shock were used to identify PfAP2-HS as a transcription factor that is essential for survival at febrile temperatures. Transcriptomic analysis was performed to compare the effect of heat shock in parasites presenting the wild type form of PfAP2-HS (10E) and parasites that have defects in this protein, either a premature stop codon mutation (10G) or the deletion of the entire pfap2-hs gene (10E_pfap2-hs). A timecourse analysis including samples taken before, during and after heat shock revealed that the initial phase of the PfAP2-HS-dependent response is largely restricted to hsp70-1 and hsp90.
2021-05-17 | GSE149392 | GEO
Project description:RNA-seq and ribosome footprinting libraries of mouse 3T3 and human 293T cellsrelated to Shalgi et al. 2013 36bases paired-end RNA-seq, and ribosome footprinting libraries for: 3T3 cells - Control, 8 hours of mild heat shock (42) and 2 hours of severe heat shock (44) - in replicates, as well as 3T3 cells treated by mild followed by severe heat shock. In addition, 3T3 cells treated with Hsp70 inhibitor VER-155008 (Massey et al. 2010), and 293T cells transfected with Hspa1a or GFP, before and after 2 hours of severe heat shock.
2013-01-03 | E-GEOD-32060 | biostudies-arrayexpress
Project description:The Heat Shock response (HSR) is a highly conserved transcriptional program induced by the exposure to a variety of environmental stressors. Following an insult, a small subset of genes, known as the Heat Shock genes, are rapidly induced by the Heat Shock Factors (HSFs) to maintain protein homeostasis and ensure cell survival. In parallel, a large portion of the genome becomes repressed. HS associated global gene repression is still largely poorly understood. In this study, we demonstrate that transcription downregulation during Heat shock is mainly achieved by premature transcription termination through the disruption of telescripting.
2022-01-24 | GSE189562 | GEO