Heat Hardening
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
SUBMITTER: Eugene Schuster
PROVIDER: E-MTAB-1608 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Experiment was designed to identify transcriptome changes during cold acclimation of Drosophila melanogaster male flies. Resistance to cold is often measured by recovery times from chill coma, which is induced almost immediately upon exposure to low but non-freezing temperatures (~0C), with flies becoming immobilised and losing motor activity. This paralysis is also ostensibly reversible upon return to normal temperatures, although again there can be longer term effects. Acclimation for increased cold resistance requires exposure periods ranging from hours or days to several weeks at low temperatures between 0C to 12C, and samples were taken during the cold acclimation period (1 hr, 2 hr, 3 hr, 6 hr, 12 hr, 24 hr, 36 hr and 48 hr).
2014-05-01 | E-MTAB-1607 | biostudies-arrayexpress
Project description:Cold hardening treatment, a brief exposure to low temperatures (e.g. 0°C for 2 h), can protect certain insects against subsequent exposure to temperatures sufficiently low to cause damage or lethality. Microarray analysis to examine the changes in transcript abundance associated with cold hardening has been undertaken in Drosophila melanogaster in order to gain insight into this phenomenon. Transcripts associated with 36 genes were identified, a subset of which appeared to be also differentially expressed after heat shock treatment. Quantitative RT-PCR was used to independently determine transcript abundance of a subset of these sequences. Taken together, these assays suggest that stress proteins, including Hsp23, Hsp26, Hsp83 and Frost as well as membrane-associated proteins may contribute to the cold hardening response. Co-reared flies were separated into a control group and a treatment group at random. RNA was isolated from the cold-shocked flies and the respective controls and was used for direct comparisons on cDNA microarrays. Treatments were not varied as they had been optimized in previous studies. A pilot experiment was performed using the Drosophila 7k2 array (GPL311) and subsequently three pairs of independent biological samples were evaluated with the Drosophila 12k1 array (GPL1467).
2005-11-30 | E-GEOD-2989 | biostudies-arrayexpress
Project description:Cold hardening treatment, a brief exposure to low temperatures (e.g. 0°C for 2 h), can protect certain insects against subsequent exposure to temperatures sufficiently low to cause damage or lethality. Microarray analysis to examine the changes in transcript abundance associated with cold hardening has been undertaken in Drosophila melanogaster in order to gain insight into this phenomenon. Transcripts associated with 36 genes were identified, a subset of which appeared to be also differentially expressed after heat shock treatment. Quantitative RT-PCR was used to independently determine transcript abundance of a subset of these sequences. Taken together, these assays suggest that stress proteins, including Hsp23, Hsp26, Hsp83 and Frost as well as membrane-associated proteins may contribute to the cold hardening response. Keywords: cold stress response
2005-12-01 | GSE2989 | GEO
Project description:Temperature is an important ecological condition, and sudden temperature changes in soil can induce stress in soil-dwelling invertebrates. Soil animals can move to more favorable habitats and/or adapt physiologically to a stressful environment. Hyperthermic conditions will impact gene expression as one of the first steps. We use a transcriptomics approach to identify the transcripts of which expression changed in response to heat stress in the springtail Folsomia candida using a 5,131 probe microarray. A temperature shift from 20°C to 30°C for 30 minutes significantly altered the expression of 142 genes, of which 116 were upregulated, and 26 downregulated. Many upregulated genes encoded heat shock proteins (Hsps) or enzymes involved in the synthesis of ATP, such as members of the electron transport chain. Furthermore, genes involved in oxidative stress and anion-transporting ATPases were upregulated. Downregulated were glycoside hydrolases, involved in catalysis of certain disaccharides, which indicate an accumulation of stress-protective disaccharides. The microarray results from this study, which were validated using quantitative RT PCR, reveal a mild response to heat shock in this soil invertebrate, relative to other organisms. This may be due to specific ecological factors during evolution of soil invertebrates, such as the relatively stable temperatures in the soil habitat. This study presents potential candidate genes for future functional studies concerning thermal stress in soil-dwelling invertebrates, like e.g., the investigation of the heat hardening process. Folsomia candida was first acclimated to LUFA 2.2 soil at 20 C for two days. Then animals were either exposed to 30 C for 30 minutes (heat shock treated), or were not heat shocked (reference). For each treatment 4 biological replicates were used, replicate samples consisted of total RNA extracted from ~30 animals exposed in the same jar to either reference or heat shock. Each unique heat shock treated sample was hybridized to a unique reference sample. In total in 4 hybridizations of 8 samples, was performed. The dyes were evenly distributed, which means that for each treatment two samples were labeled with cy3 and the other two with cy5.
2010-06-24 | E-GEOD-17024 | biostudies-arrayexpress
Project description:Although significant work has been undertaken regarding the response of model and crop plants to heat shock during the acclimatory phase, few studies have examined the steady state response to the mild heat stress encountered in temperate agriculture. In the present work we therefore exposed tuberising potato plants to mildly elevated temperatures (30/20C), day/night) for up to five weeks and compared tuber yield, physiological and biochemical responses, and leaf and tuber metabolomes and transcriptomes with plants grown under optimal conditions (22/16C). Growth at elevated temperature reduced tuber yield despite an increase in net foliar photosynthesis. This was associated with major shifts in leaf and tuber metabolite profiles, a significant decrease in leaf glutathione redox state and decreased starch synthesis in tubers. Furthermore, growth at elevated temperature had a profound impact on leaf and tuber transcript expression with large numbers of transcripts displaying a rhythmic oscillation at the higher growth temperature. RT-PCR revealed perturbation in the expression of circadian clock transcripts including StSP6A, previously identified as a tuberisation signal. Our data indicate that potato plants grown at moderately elevated temperatures do not exhibit classic symptoms of abiotic stress but that tuber development responds via a diversity of biochemical and molecular signals. In this submission we are looking at gene expression changes with respect to both temperature and time, every 4h over a 24h period whereby diurnal changes may be apparent.
2013-08-01 | E-MTAB-1655 | biostudies-arrayexpress
Project description:This experiment aims at investigating the effects of heat-stress on transcriptomic changes of the muscle cells in in-vitro model using the mouse myoblast cell line C2C12. Four incubation temperatures were set as a treatment condition at 35°C (cold stress), 37°C (control), 39°C (mild heat stress) and 41°C (severe heat stress). The cells were cultured under the treatment conditions for 72 hours prior to harvesting the cells for RNA extraction. The experiment was done in three independent replications.
2024-11-30 | E-MTAB-9895 | biostudies-arrayexpress
Project description:The ability to rapidly respond to changes in temperature is critical for insects and other ectotherms living in variable environments. In a physiological process termed rapid cold-hardening (RCH), exposure to non-lethal low temperature allows many insects to significantly increase their cold tolerance in a matter of minutes to hours. Additionally, there are rapid changes in gene expression and cell physiology during recovery from cold injury, and we hypothesize that RCH may modulate some of these processes during recovery. In this study, we used a cDNA microarray to examine the molecular mechanisms of RCH and cold shock (CS) recovery in the flesh fly, Sarcophaga bullata. With our custom 2-color array, we measured expression of ~15,000 ESTs during RCH and during recovery from cold shock. Surprisingly, no transcripts were upregulated during RCH, and likewise, RCH had a minimal effect on the transcript signature during recovery from cold shock. However, during recovery from cold shock, we observed differential expression of ~1,400 ESTs, including a number of heat shock proteins, cytoskeletal components, and genes from several cell signaling pathways. Several gene pathways correlated well with metabolomics data, indicating that coordinated changes in gene expression and metabolism contribute to recovery from cold shock. Four treatment groups (C, RCH, CS+2R, RCH+CS+2R), four biological replicates of four pooled individuals for each treatment. Each phenotype was hybridized with the control, and the CS+2R and RCH+CS+2R groups were also hybridized together.
2012-03-14 | E-GEOD-36483 | biostudies-arrayexpress
Project description:Background: The in vivo gene response associated with hyperthermia and subsequent return to homeostasis or development of heat illness is poorly understood. Early activation of gene networks in the heat stress response is likely to lead to the systemic inflammation, multi-organ functional impairment, and other pathophysiological states characteristic of heat illness. Here, we perform an unbiased global characterization of the multi-organ gene response using an in vivo model of heat stress in the conscious rat. Results: Rats were subjected to elevated temperatures until implanted thermal probes indicated a maximal core temperature of 41.8 M-BM-0C (Tc,Max). Liver, lung, kidney, and heart were harvested at Tc,Max, 24 hours, and 48 hours after heat stress in groups of experimental animals and time-matched controls kept at ambient temperature. Clinical chemistries suggested abnormal function in liver, kidney, and lung at Tc,Max, and cardiac histopathology at 48 hours supported persistent cardiac damage in 3 out of 6 animals. Microarray analysis identified 78 differentially expressed genes common to all 4 organs at Tc,Max (i.e., the consensus heat stress response). Gene set enrichment analysis of gene ontology terms identified 25 biological processes in 4 general gene ontology categories: protein folding, regulation of apoptosis, response to cytokines, and transcriptional responses. Functional analysis clustering of the 78 differentially expressed genes in the consensus heat stress response also identified functional categories of protein folding and regulation of apoptosis. Self-organizing maps identified gene-specific signatures corresponding to protein folding disorders specific to only heat-stressed rats with histopathologic evidence of cardiac injury at 48 hours. Enrichment analysis of differentially expressed proteins in heat-injured hearts at 48 hours corroborated gene enrichment analysis results. Quantitative proteomics analysis by iTRAQ demonstrated that differential protein expression was not comparable to transcript expression at Tc,Max and 24 hours. However, the profile of differentially expressed proteins closely matched the transcriptomic profile in heat-injured animals at 48 hours. Pathway analysis at both the transcript and protein levels supported catastrophic deficits in energetics and cellular metabolism, chronic proteotoxic response, and activation of the unfolded protein response. Calculation of protein super-saturation scores demonstrated an increased propensity of proteins to aggregate in the hearts of heat-injured animals at 48 hours, consistent with accumulation of misfolded proteins. Conclusions: Global transcriptomic and proteomic analysis identified networks of genes and proteins initiating an unfolded protein response, metabolic dysfunction, and mitochondrial energy crisis in animals with histopathologic evidence of persistent heat injury, providing the basis for a systems-level physiological model of heat illness and recovery. To induce the pathophysiological effects of heat stress, conscious rats were placed in an incubator at 37M-BM-:C and their core temperature was monitored. Animals were sacrificed when their core temperature reached 41.8M-BM-:C (Tc,Max), or they were returned to their normal housing environment and were allowed to recover for up to 24 or 48 hours prior to sacrifice. Time-matched controls were euthanized at times corresponding to Tc,Max, 24 hours, and 48 hours. For each condition n=6 for a total of 36 animals. Four tissues (liver, lung, kidney and heart) were analyzed from each animal for a total of 144 arrays; however a few arrays did not pass QC therefore only 140 are reported here: 34 liver, 35 lung, 36 kidney, or 35 heart.
2015-01-14 | E-GEOD-56740 | biostudies-arrayexpress
Project description:The conventional view is that high temperatures cause microorganisms to replicate slowly or die. In this view, microorganisms autonomously combat heat-induced damage. However, microorganisms co-exist with each other, which raises the underexplored and timely question of whether microorganisms can cooperatively combat heat-induced damages at high temperatures. Here, we use the budding yeast Saccharomyces cerevisiae to show that cells can help each other and their future generations to survive and replicate at high temperatures. As a consequence, even at the same temperature, a yeast population can exponentially grow, never grow or grow after unpredictable durations (hours to days) of stasis, depending on its population density. Through the same mechanism, yeasts collectively delay and can eventually stop their approach to extinction, with higher population densities stopping faster. These features arise from yeasts secreting and extracellularly accumulating glutathione—a ubiquitous heat-damage-preventing antioxidant. We show that the secretion of glutathione, which eliminates harmful extracellular chemicals, is both necessary and sufficient for yeasts to collectively survive at high temperatures. A mathematical model, which is generally applicable to any cells that cooperatively replicate by secreting molecules, recapitulates all of these features. Our study demonstrates how organisms can cooperatively define and extend the boundaries of life-permitting temperatures.
2020-03-24 | GSE137151 | GEO
Project description:We used microarrays to investigate the transcriptome of 6 days old male flies exposed to either 15 or 25 C development at either constant or fluctuating temperatures. Further, we investigated gene expression at benign (20C) and high (35C) temperatures With global climate change temperature means and variability are expected to increase. Thus, exposures to elevated temperatures are expected to become an increasing challenge for terrestrial ectotherm populations. While evolutionary adaptation seems to be constrained or proceed at an insufficient pace, many populations are expected to rely on phenotypic plasticity (thermal acclimation) for coping with the predicted changes. However, the effects of fluctuating temperature on the molecular mechanisms and the implications for heat tolerance are not well understood. To understand and predict consequences of climate change it is important to investigate how different components of the thermal environment, including fluctuating thermal conditions, contribute to changes in thermal acclimation. In this study we investigated the impact of mean and diurnal fluctuation of temperature on heat tolerance in Drosophila melanogaster and on the underlying molecular mechanisms in adult male flies. Flies from two constant and two ecologically relevant fluctuating temperature regimes were tested for their critical thermal maxima (CTmax) and associated global gene expression profiles at benign and thermally stressful conditions. Both temperature parameters contributed independently to the thermal acclimation, with regard to heat tolerance as well as the global gene expression profile. Although the independent transcriptional effects caused by fluctuations were relatively small, they are likely to be essential for our understanding of thermal adaptation. Thus, high temperature acclimation ability might not be measured correctly and might even be underestimated at constant temperatures. Our data suggests that the particular mechanisms affected by thermal fluctuations are related to phototransduction and environmental sensing. Thus genes and pathways involved in those processes are likely to be of major importance in a future warmer and more fluctuating climate. Eight experimental groups were analyzed in triplicate, in total 24 Affymetrix GeneChip Drosophila Genome 2.0 Arrays
2016-08-05 | E-GEOD-84680 | biostudies-arrayexpress