Induction of heat-shock (stress) protein gene expression by selected natural and anthropogenic disturbances in the octocoral Dendronephthya klunzingeri

2000 ◽  
Vol 245 (2) ◽  
pp. 265-276 ◽  
Author(s):  
Matthias Wiens ◽  
Mohammed S.A Ammar ◽  
Ahmed H Nawar ◽  
Claudia Koziol ◽  
Hamdy M.A Hassanein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Protein Gene ◽  
Stress Protein ◽  
Anthropogenic Disturbances ◽  
Heat Shock Stress ◽  
Shock Stress

scholarly journals Direct link between metabolic regulation and the heat-shock response through the transcriptional regulator PGC-1α

2015 ◽  
Vol 112 (42) ◽  
pp. E5669-E5678 ◽  
Author(s):  
Neri Minsky ◽  
Robert G. Roeder
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Heat Shock ◽  
Metabolic Regulation ◽  
Hormone Receptors ◽  
Transcriptional Networks ◽  
Direct Link ◽  
Heat Shock Stress ◽  
Metabolic Genes ◽  
Shock Stress

In recent years an extensive effort has been made to elucidate the molecular pathways involved in metabolic signaling in health and disease. Here we show, surprisingly, that metabolic regulation and the heat-shock/stress response are directly linked. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a critical transcriptional coactivator of metabolic genes, acts as a direct transcriptional repressor of heat-shock factor 1 (HSF1), a key regulator of the heat-shock/stress response. Our findings reveal that heat-shock protein (HSP) gene expression is suppressed during fasting in mouse liver and in primary hepatocytes dependent on PGC-1α. HSF1 and PGC-1α associate physically and are colocalized on several HSP promoters. These observations are extended to several cancer cell lines in which PGC-1α is shown to repress the ability of HSF1 to activate gene-expression programs necessary for cancer survival. Our study reveals a surprising direct link between two major cellular transcriptional networks, highlighting a previously unrecognized facet of the activity of the central metabolic regulator PGC-1α beyond its well-established ability to boost metabolic genes via its interactions with nuclear hormone receptors and nuclear respiratory factors. Our data point to PGC-1α as a critical repressor of HSF1-mediated transcriptional programs, a finding with possible implications both for our understanding of the full scope of metabolically regulated target genes in vivo and, conceivably, for therapeutics.

scholarly journals Ischemia of the dog heart induces the appearance of a cardiac mRNA coding for a protein with migration characteristics similar to heat-shock/stress protein 71.

1986 ◽  
Vol 59 (1) ◽  
pp. 110-114 ◽  
Author(s):  
W H Dillmann ◽  
H B Mehta ◽  
A Barrieux ◽  
B D Guth ◽  
W E Neeley ◽  
...  
Keyword(s):  
Heat Shock ◽  
Stress Protein ◽  
Dog Heart ◽  
Heat Shock Stress ◽  
Shock Stress

scholarly journals Gene Expression Profiling ofClostridium botulinumunder Heat Shock Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Wan-dong Liang ◽  
Yun-tian Bi ◽  
Hao-yan Wang ◽  
Sheng Dong ◽  
Ke-shen Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Environmental Changes ◽  
Expression Patterns ◽  
Trna Synthetase ◽  
Ph Change ◽  
Heat Shock Stress ◽  
Shock Stress

During growth,C. botulinumis always exposed to different environmental changes, such as temperature increase, nutrient deprivation, and pH change; however, its corresponding global transcriptional profile is uncharacterized. This study is the first description of the genome-wide gene expression profile ofC. botulinumin response to heat shock stress. Under heat stress (temperature shift from 37°C to 45°C over a period of 15 min), 176C. botulinumATCC 3502 genes were differentially expressed. The response included overexpression of heat shock protein genes (dnaKoperon,groESL,hsp20,andhtpG) and downregulation of aminoacyl-tRNA synthetase genes (valS,queA,tyrR, andgatAB) and ribosomal and cell division protein genes (ftsZandftsH). In parallel, several transcriptional regulators (marR,merR, andompRfamilies) were induced, suggesting their involvement in reshuffling of the gene expression profile. In addition, many ABC transporters (oligopeptide transport system), energy production and conversion related genes (glpAandhupL), cell wall and membrane biogenesis related genes (fabZ,fabF, andfabG), flagella-associated genes (flhA,flhM,flhJ,flhS, andmotAB), and hypothetical genes also showed changed expression patterns, indicating that they may play important roles in survival under high temperatures.

756 MUSCLE HEAT SHOCK/STRESS PROTEIN CHANGES AFTER ECCENTRIC EXERCISE

1994 ◽  
Vol 26 (Supplement) ◽  
pp. S134 ◽  
Author(s):  
H. S. Thompson ◽  
S. P. Scordilis ◽  
P. M. Clarkson
Keyword(s):  
Heat Shock ◽  
Eccentric Exercise ◽  
Stress Protein ◽  
Heat Shock Stress ◽  
Shock Stress

scholarly journals A-to-I RNA Editing Affects lncRNAs Expression after Heat Shock

2018 ◽  
Author(s):  
Roni Haas ◽  
Nabeel S. Ganem ◽  
Ayya Keshet ◽  
Angela Orlov ◽  
Alla Fishman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Rna Editing ◽  
Rna Structures ◽  
Wild Type ◽  
Adenosine Deaminases ◽  
C Elegans ◽  
Heat Shock Stress ◽  
Upregulated Genes ◽  
Shock Stress

Adenosine to inosine (A-to-I) RNA editing is a highly conserved regulatory process carried out by adenosine-deaminases (ADARs) on dsRNAs. Although a considerable fraction of the transcriptome is edited, the function of most editing sites is unknown. Previous studies indicate changes in A-to-I RNA editing frequencies following exposure to several stress types. However, the overall effect of stress on the expression of ADAR targets is not fully understood. Here, we performed high-throughput RNA sequencing of wild-type and ADAR mutant C. elegans worms after heat-shock to analyze the effect of heat-shock stress on the expression pattern of genes. We found that ADAR regulation following heat-shock does not directly involve heat-shock related genes. Our analysis also revealed that lncRNAs and pseudogenes, which have a tendency for secondary RNA structures, are enriched among upregulated genes following heat-shock in ADAR mutant worms. The same group of genes is downregulated in ADAR mutant worms under permissive conditions, which is likely, considering that A-to-I editing protects endogenous dsRNA from RNA-interference (RNAi). Therefore, temperature increases may destabilize dsRNA structures and protect them from RNAi degradation, despite the lack of ADAR function. These findings shed new light on the dynamics of gene expression under heat-shock in relation to ADAR function.

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