Histone Methylation and Modulation of Gene Expression in Response to Heat Shock and Chemical Stress in Drosophila

Author(s):  
Robert M. Tanguay ◽  
Richard Desrosiers
1994 ◽  
Vol 107 (8) ◽  
pp. 2209-2214 ◽  
Author(s):  
R.Y. Liu ◽  
P.M. Corry ◽  
Y.J. Lee

We have investigated the regulation mechanism of chemical stress-induced hsp70 gene expression in murine L929 cells. Our data show that chemical treatments including sodium arsenite, cadmium chloride and sodium salicylate, induced significant synthesis of hsp70 and its mRNA. The induced hsp70 gene expression appears to be regulated at the transcriptional level. A factor (CHBF), which constitutively binds to the heat shock element (HSE) at 37 degrees C, functions like a negative regulator and the heat-induced heat shock factor (HSF) acts as an activator. The chemical treatments that induce significant hsp70 synthesis activate HSF binding to HSE but also dissociate the HSE-CHBF complex. Some chemical treatments, e.g. IPTG, which fail to activate hsp70 gene transcription, still activate HSF binding to HSE. However, in this case, the HSE-CHBF complex remained like that of untreated control cells.


Animals ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 97
Author(s):  
Matteo Zarantoniello ◽  
Martina Bortoletti ◽  
Ike Olivotto ◽  
Stefano Ratti ◽  
Carlo Poltronieri ◽  
...  

The present study aimed to investigate the acute response of gilthead seabream (Sparus aurata) juveniles exposed to temperature, salinity and ammonia stress. Radioimmunoassay was used to evaluate cortisol levels, whereas insulin-like growth factors (igf1 and igf2), myostatin (mstn), heat-shock protein 70 (hsp70) and glucocorticoid receptor (gr) gene expression was assessed trough Real-Time PCR. The presence and localization of IGF-I and HSP70 were investigated by immunohistochemistry. In all the stress conditions, a significant increase in cortisol levels was observed reaching higher values in the thermic and chemical stress groups. Regarding fish growth markers, igf1 gene expression was significantly higher only in fish subjected to heat shock stress while, at 60 min, igf2 gene expression was significantly lower in all the stressed groups. Temperature and ammonia changes resulted in a higher mstn gene expression. Molecular analyses on stress response evidenced a time dependent increase in hsp70 gene expression, that was significantly higher at 60 min in fish exposed to heat shock and chemical stress. Furthermore, the same experimental groups were characterized by a significantly higher gr gene expression respect to the control one. Immunostaining for IGF-I and HSP70 antibodies was observed in skin, gills, liver, and digestive system of gilthead seabream juveniles.


2017 ◽  
Author(s):  
Tania Pereira ◽  
Ester Vilaprinyo ◽  
Gemma Belli ◽  
Enric Herrero ◽  
Baldiri Salvado ◽  
...  

AbstractMicroorganisms evolved adaptive responses that enable them to survive stressful challenges in ever changing environments by adjusting metabolism through the modulation of gene expression, protein levels and activity, and flow of metabolites. More frequent challenges allow natural selection ampler opportunities to select from a larger number of phenotypes that are compatible with survival. Understanding the causal relationships between physiological and metabolic requirements that are needed for cellular stress adaptation and gene expression changes that are used by organisms to achieve those requirements may have a significant impact in our ability to interpret and/or guide evolution.Here, we study those causal relationships during heat shock adaptation in the yeast Saccharomyces cerevisiae. We do so by combining dozens of independent experiments measuring whole genome gene expression changes during stress response with a nonlinear simplified kinetic model of central metabolism.This combination is used to create a quantitative, multidimensional, genotype-to-phenotype mapping of the metabolic and physiological requirements that enable cell survival to the feasible changes in gene expression that modulate metabolism to achieve those requirements. Our results clearly show that the feasible changes in gene expression that enable survival to heat shock are specific for this stress. In addition, they suggest that genetic programs for adaptive responses to desiccation/rehydration and to pH shifts might be selected by physiological requirements that are qualitatively similar, but quantitatively different to those for heat shock adaptation. In contrast, adaptive responses to other types of stress do not appear to be constrained by the same qualitative physiological requirements. Our model also explains at the mechanistic level how evolution might find different sets of changes in gene expression that lead to metabolic adaptations that are equivalent in meeting physiological requirements for survival. Finally, our results also suggest that physiological requirements for heat shock adaptation might be similar between unicellular ascomycetes that live in similar environments. Our analysis is likely to be scalable to other adaptive response and might inform efforts in developing biotechnological applications to manipulate cells for medical, biotechnological, or synthetic biology purposes.


2019 ◽  
Vol 70 (19) ◽  
pp. 5355-5374 ◽  
Author(s):  
Dandan Zang ◽  
Jingxin Wang ◽  
Xin Zhang ◽  
Zhujun Liu ◽  
Yucheng Wang

Abstract Plant heat shock transcription factors (HSFs) are involved in heat and other abiotic stress responses. However, their functions in salt tolerance are little known. In this study, we characterized the function of a HSF from Arabidopsis, AtHSFA7b, in salt tolerance. AtHSFA7b is a nuclear protein with transactivation activity. ChIP-seq combined with an RNA-seq assay indicated that AtHSFA7b preferentially binds to a novel cis-acting element, termed the E-box-like motif, to regulate gene expression; it also binds to the heat shock element motif. Under salt conditions, AtHSFA7b regulates its target genes to mediate serial physiological changes, including maintaining cellular ion homeostasis, reducing water loss rate, decreasing reactive oxygen species accumulation, and adjusting osmotic potential, which ultimately leads to improved salt tolerance. Additionally, most cellulose synthase-like (CSL) and cellulose synthase (CESA) family genes were inhibited by AtHSFA7b; some of them were randomly selected for salt tolerance characterization, and they were mainly found to negatively modulate salt tolerance. By contrast, some transcription factors (TFs) were induced by AtHSFA7b; among them, we randomly identified six TFs that positively regulate salt tolerance. Thus, AtHSFA7b serves as a transactivator that positively mediates salinity tolerance mainly through binding to the E-box-like motif to regulate gene expression.


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