scholarly journals Stressed out underground?: Transcriptomics illuminates the genome-wide response to heat stress in surface and subterranean diving beetles

2021 ◽  
Author(s):  
Perry G Beasley-Hall ◽  
Terry Bertozzi ◽  
Tessa M Bradford ◽  
Charles S P Foster ◽  
Karl Jones ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Thermal Tolerance ◽  
Molecular Level ◽  
Differential Expression Analysis ◽  
Increased Risk ◽  
Shock Response ◽  
The Face ◽  
Surface Dwelling

Subterranean habitats are environmentally stable with respect to temperature, humidity, and the absence of light. The transition to a subterranean lifestyle might therefore be expected to cause considerable shifts in an organism's physiology; here, we investigate how subterranean colonisation affects thermal tolerance. Subterranean organisms might be at an increased risk of decline in the face of global temperature rises, but robust data on the fauna is lacking, particularly at the molecular level. In this study we compare the heat shock response of two species of diving beetle in the genus Paroster: one surface-dwelling (P. nigroadumbratus), the other restricted to a single aquifer (P. macrosturtensis). P. macrosturtensis has been previously established as having a lower thermal tolerance compared to surface-dwelling relatives, but the genomic basis of this difference is unknown. By sequencing transcriptomes of experimentally heat-shocked individuals and performing differential expression analysis, we demonstrate both species can mount a heat shock response at high temperatures (35C), in agreement with past survival experiments. However, the genes involved in these responses differ between species, and far greater genes are differentially expressed in the surface species, which may explain its more robust response to heat stress. In contrast, the subterranean species significantly upregulated the heat shock protein gene Hsp68 in the experimental setup under conditions it would likely encounter in nature (25C), suggesting it may be more sensitive to ambient stressors, e.g. handling. The results presented here contribute to an emerging narrative concerning weakened thermal tolerances in obligate subterranean organisms at the molecular level.

scholarly journals Molecular Basis of the Defective Heat Stress Response in Mycobacterium leprae

2007 ◽  
Vol 189 (24) ◽  
pp. 8818-8827 ◽  
Author(s):  
Diana L. Williams ◽  
Tana L. Pittman ◽  
Mike Deshotel ◽  
Sandra Oby-Robinson ◽  
Issar Smith ◽  
...  
Keyword(s):  
Heat Stress ◽  
Stress Response ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Elevated Temperatures ◽  
Transcriptional Response ◽  
Mycobacterium Leprae ◽  
Heat Stress Response ◽  
Regulatory Circuits ◽  
Shock Response

ABSTRACT Mycobacterium leprae, a major human pathogen, grows poorly at 37°C. The basis for its inability to survive at elevated temperatures was investigated. We determined that M. leprae lacks a protective heat shock response as a result of the lack of transcriptional induction of the alternative sigma factor genes sigE and sigB and the major heat shock operons, HSP70 and HSP60, even though heat shock promoters and regulatory circuits for these genes appear to be intact. M. leprae sigE was found to be capable of complementing the defective heat shock response of mycobacterial sigE knockout mutants only in the presence of a functional mycobacterial sigH, which orchestrates the mycobacterial heat shock response. Since the sigH of M. leprae is a pseudogene, these data support the conclusion that a key aspect of the defective heat shock response in M. leprae is the absence of a functional sigH. In addition, 68% of the genes induced during heat shock in M. tuberculosis were shown to be either absent from the M. leprae genome or were present as pseudogenes. Among these is the hsp/acr2 gene, whose product is essential for M. tuberculosis survival during heat shock. Taken together, these results suggest that the reduced ability of M. leprae to survive at elevated temperatures results from the lack of a functional transcriptional response to heat shock and the absence of a full repertoire of heat stress response genes, including sigH.

Sub-lethal heat stress causes apoptosis in an Antarctic fish that lacks an inducible heat shock response

2014 ◽  
Vol 44 ◽  
pp. 119-125 ◽  
Author(s):  
Isaac M. Sleadd ◽  
Marissa Lee ◽  
Daniel O. Hassumani ◽  
Tonya M.A. Stecyk ◽  
Otto K. Zeitz ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Antarctic Fish ◽  
Shock Response

scholarly journals Effect of single and repeated heat stress on chemical signals of heat shock response cascade in the rat’s heart

2017 ◽  
Vol 23 (4) ◽  
pp. 561-570 ◽  
Author(s):  
Gordana Ilievska ◽  
Suzana Dinevska-Kjovkarovska ◽  
Biljana Miova
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Chemical Signals ◽  
Shock Response

scholarly journals The heat shock response in HeLa cells is accompanied by elevated expression of the c-fos proto-oncogene.

1987 ◽  
Vol 7 (10) ◽  
pp. 3452-3458 ◽  
Author(s):  
G K Andrews ◽  
M A Harding ◽  
J P Calvet ◽  
E D Adamson
Keyword(s):  
Heavy Metals ◽  
Protein Synthesis ◽  
Heat Stress ◽  
Heat Shock ◽  
Hela Cells ◽  
Heat Shock Response ◽  
Mrna Level ◽  
Hsp 70 ◽  
Shock Response ◽  
Elevated Expression

Several known inducers of the heat shock response (heat stress, arsenite, and heavy metals) were shown to cause a significant elevation of c-fos mRNA in HeLa cells. Heat stress resulted in a time- and temperature-dependent prolonged elevation in the level of c-fos mRNA, which was accompanied by increased translation of c-fos protein and its appearance in the nucleus. Elevated expression of c-fos during heat stress was paralleled by induction of hsp 70 mRNA, while levels of c-myc and metallothionein mRNAs declined. Treatment of HeLa cells with arsenite or heavy metals also resulted in increased levels of hsp 70, as well as c-fos mRNA. Although elevated expression of c-fos was prevented by inhibitors of RNA synthesis, analysis of relative rates of gene transcription showed that during heat stress there was a negligible change in c-fos transcription. Therefore, the enhanced expression of c-fos during the heat shock response is likely to occur primarily through posttranscriptional processes. Cycloheximide was also shown to significantly increase the c-fos mRNA level in HeLa cells. There results are consistent with the observation that these inducers of the heat shock response, as well as cycloheximide, repress protein synthesis and suggest that the increase in the level of c-fos mRNA is caused by an inhibition of protein synthesis. This supports the hypothesis that c-fos mRNA is preferentially stabilized under conditions which induce the heat shock response, perhaps by decreased synthesis of a short-lived protein which regulates c-fos mRNA turnover.

The Heat-Shock Response and Expression of Heat-Shock Proteins in Wheat Under Diurnal Heat Stress and Field Conditions

1994 ◽  
Vol 21 (6) ◽  
pp. 857 ◽  
Author(s):  
HT Nguyen ◽  
CP Joshi ◽  
N Klueva ◽  
J Weng ◽  
KL Hendershot ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Heat Tolerance ◽  
Heat Shock Response ◽  
Field Conditions ◽  
Shock Response ◽  
Heat Tolerant ◽  
Shock Proteins

The occurrence of heat-shock proteins (HSPs) in response to high temperature stress is a universal phenomenon in higher plants and has been well documented. However, in agriculturally important species, less is known about the expression of HSPs under natural environments. A review of the heat-shock response in wheat (Triticum aestivum L.) is presented and recent results on the expression of wheat HSPs under diurnal stress and field conditions are reported. In the field experiment, flag leaf blade temperatures were obtained and leaf blades collected for northern blot analysis using HSP 16.9 cDNA as a probe. Temperatures of leaf blades ranged from 32 to 35�C under the tested field conditions at New Deal near Lubbock, Texas. Messenger RNAs encoding a major class of low molecular weight HSPs, HSP 16.9, were detected in all wheat genotypes examined. The results suggested that HSPs are synthesised in response to heat stress under agricultural production, and furthermore, that HSPs are produced in wheats differing in geographic background. In the controlled growth chamber experiment, HSP expression in two wheat cultivars, Mustang (heat tolerant) and Sturdy (heat susceptible) were analysed to determine if wheat genotypes differing in heat tolerance differ in in vitro HSP synthesis (translatable HSP mRNAs) under a chronic, diurnal heat-stress regime. Leaf tissues were collected from seedlings over a time-course and poly (A)+RNAs were isolated for in vitro translation and 2-D gel electrophoresis. The protein profiles shown in the 2-D gel analysis revealed that there were not only quantitative differences of individual HSPs between these two wheat lines, but also some unique HSPs which were only found in the heat tolerant line. This data provides evidence of a correlation between HSP synthesis and heat tolerance in wheat under a simulated field environment and suggests that further genetic analysis of HSPs in a segregating population is worthy of investigation. In conclusion, the results of this study provide an impetus for the investigation of the roles of HSP genes in heat tolerance in wheat.

Heat shock response of killifish (Fundulus heteroclitus): candidate gene and heterologous microarray approaches

2010 ◽  
Vol 41 (2) ◽  
pp. 171-184 ◽  
Author(s):  
Timothy M. Healy ◽  
Wendy E. Tymchuk ◽  
Edward J. Osborne ◽  
Patricia M. Schulte
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Heat Shock Response ◽  
Thermal Tolerance ◽  
Fundulus Heteroclitus ◽  
Swimming Performance ◽  
Shock Response ◽  
Shock Proteins ◽  
Heterologous Microarray

Northern and southern subspecies of the Atlantic killifish, Fundulus heteroclitus, differ in maximal thermal tolerance. To determine whether these subspecies also differ in their heat shock response (HSR), we exposed 20°C acclimated killifish to a 2 h heat shock at 34°C and examined gene expression in fish from both subspecies during heat shock and recovery using real-time quantitative PCR and a heterologous cDNA microarray designed for salmonid fishes. The heat shock proteins Hsp70-1, hsp27, and hsp30 were upregulated to a greater extent in the high temperature-tolerant southern subspecies than in the less tolerant northern subspecies, whereas hsp70-2 (which showed the largest upregulation of all the heat shock proteins) in both gill and muscle and hsp90α in muscle was upregulated to a greater extent in northern than in southern fish. These data demonstrate that differences in the HSR between subspecies cannot be due to changes in a single global regulator but must occur via gene-specific mechanisms. They also suggest that the role, if any, of hsps in establishing thermal tolerance is complex and varies from gene to gene. Heterologous microarray hybridization provided interpretable gene expression signatures, detecting differential regulation of genes known to be involved in the heat shock response in other species. Under control conditions, a variety of genes were differentially expressed in muscle between subspecies that suggest differences in muscle fiber type and could relate to previously observed differences between subspecies in the thermal sensitivity of swimming performance and metabolism.

scholarly journals CHIP mutations affect the heat shock response differently in human fibroblasts and iPSC-derived neurons

2020 ◽  
Vol 13 (10) ◽  
pp. dmm045096
Author(s):  
S. Schuster ◽  
E. Heuten ◽  
A. Velic ◽  
J. Admard ◽  
M. Synofzik ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Cortical Neurons ◽  
Human Fibroblasts ◽  
Cerebellar Atrophy ◽  
Spinocerebellar Ataxia Type ◽  
Control Line ◽  
Ataxic Gait ◽  
Shock Response

ABSTRACTC-terminus of HSC70-interacting protein (CHIP) encoded by the gene STUB1 is a co-chaperone and E3 ligase that acts as a key regulator of cellular protein homeostasis. Mutations in STUB1 cause autosomal recessive spinocerebellar ataxia type 16 (SCAR16) with widespread neurodegeneration manifesting as spastic-ataxic gait disorder, dementia and epilepsy. CHIP−/− mice display severe cerebellar atrophy, show high perinatal lethality and impaired heat stress tolerance. To decipher the pathomechanism underlying SCAR16, we investigated the heat shock response (HSR) in primary fibroblasts of three SCAR16 patients. We found impaired HSR induction and recovery compared to healthy controls. HSPA1A/B transcript levels (coding for HSP70) were reduced upon heat shock but HSP70 remained higher upon recovery in patient- compared to control-fibroblasts. As SCAR16 primarily affects the central nervous system we next investigated the HSR in cortical neurons (CNs) derived from induced pluripotent stem cells of SCAR16 patients. We found CNs of patients and controls to be surprisingly resistant to heat stress with high basal levels of HSP70 compared to fibroblasts. Although heat stress resulted in strong transcript level increases of many HSPs, this did not translate into higher HSP70 protein levels upon heat shock, independent of STUB1 mutations. Furthermore, STUB1(−/−) neurons generated by CRISPR/Cas9-mediated genome editing from an isogenic healthy control line showed a similar HSR to patients. Proteomic analysis of CNs showed dysfunctional protein (re)folding and higher basal oxidative stress levels in patients. Our results question the role of impaired HSR in SCAR16 neuropathology and highlight the need for careful selection of proper cell types for modeling human diseases.

scholarly journals Thermotolerance and heat acclimation may share a common mechanism in humans

2011 ◽  
Vol 301 (2) ◽  
pp. R524-R533 ◽  
Author(s):  
Matthew Kuennen ◽  
Trevor Gillum ◽  
Karol Dokladny ◽  
Edward Bedrick ◽  
Suzanne Schneider ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Heat Acclimation ◽  
Body Temperatures ◽  
Physiological Strain ◽  
Barrier Permeability ◽  
Shock Response ◽  
Gastrointestinal Barrier

Thermotolerance and heat acclimation are key adaptation processes that have been hitherto viewed as separate phenomena. Here, we provide evidence that these processes may share a common basis, as both may potentially be governed by the heat shock response. We evaluated the effects of a heat shock response-inhibitor (quercetin; 2,000 mg/day) on established markers of thermotolerance [gastrointestinal barrier permeability, plasma TNF-α, IL-6, and IL-10 concentrations, and leukocyte heat shock protein 70 (HSP70) content]. Heat acclimation reduced body temperatures, heart rate, and physiological strain during exercise/heat stress) in male subjects ( n = 8) completing a 7-day heat acclimation protocol. These same subjects completed an identical protocol under placebo supplementation (placebo). Gastrointestinal barrier permeability and TNF-α were increased on the 1st day of exercise/heat stress in quercetin; no differences in these variables were reported in placebo. Exercise HSP70 responses were increased, and plasma cytokines (IL-6, IL-10) were decreased on the 7th day of heat acclimation in placebo; with concomitant reductions in exercise body temperatures, heart rate, and physiological strain. In contrast, gastrointestinal barrier permeability remained elevated, HSP70 was not increased, and IL-6, IL-10, and exercise body temperatures were not reduced on the 7th day of heat acclimation in quercetin. While exercise heart rate and physiological strain were reduced in quercetin, this occurred later in exercise than with placebo. Consistent with the concept that thermotolerance and heat acclimation are related through the heat shock response, repeated exercise/heat stress increases cytoprotective HSP70 and reduces circulating cytokines, contributing to reductions in cellular and systemic markers of heat strain. Exercising under a heat shock response-inhibitor prevents both cellular and systemic heat adaptations.

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