The Mammalian Heat Shock (or Stress) Response: A Cellular Defense Mechanism

1987 ◽  
pp. 287-304 ◽  
Author(s):  
William J. Welch
Keyword(s):  
Stress Response ◽  
Heat Shock ◽  
Defense Mechanism ◽  
Cellular Defense

scholarly journals Modulating the Heat Stress Response to Improve Hyperthermia-Based Anticancer Treatments

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1243
Author(s):  
Enzo M. Scutigliani ◽  
Yongxin Liang ◽  
Hans Crezee ◽  
Roland Kanaar ◽  
Przemek M. Krawczyk
Keyword(s):  
Heat Stress ◽  
Stress Response ◽  
Defense Mechanism ◽  
Biological Effects ◽  
Cellular Responses ◽  
Therapeutic Window ◽  
Cancer Treatments ◽  
Heat Stress Response ◽  
Cellular Defense ◽  
Cancer Types

Cancer treatments based on mild hyperthermia (39–43 °C, HT) are applied to a widening range of cancer types, but several factors limit their efficacy and slow down more widespread adoption. These factors include difficulties in adequate heat delivery, a short therapeutic window and the acquisition of thermotolerance by cancer cells. Here, we explore the biological effects of HT, the cellular responses to these effects and their clinically-relevant consequences. We then identify the heat stress response—the cellular defense mechanism that detects and counteracts the effects of heat—as one of the major forces limiting the efficacy of HT-based therapies and propose targeting this mechanism as a potentially universal strategy for improving their efficacy.

Role of Histamine and Leucotaxin in Function of Cellular Defense Mechanism

1956 ◽  
Vol 184 (2) ◽  
pp. 296-300 ◽  
Author(s):  
László Kátó ◽  
Béla Gözsy
Keyword(s):  
Fluid Flow ◽  
Tissue Damage ◽  
Inflammatory Process ◽  
Defense Mechanism ◽  
Volatile Oils ◽  
Time Intervals ◽  
Cellular Defense ◽  
Intradermal Administration ◽  
Flow Through

Experiments are presented to the effect that in an inflammatory process histamine and leucotaxin appear successively at different and orderly time intervals, thus assuring an increased fluid flow through the capillary wall. Histamine is released not only in the inflammatory process but also by intradermal administration of such substances (volatile oils or their components) which induce neither the triple response of Th. Lewis nor any tissue damage. This could be explained by the fact that in the tissues histamine is ‘present’ but leucotaxin is ‘formed.’

scholarly journals Rox3 and Rts1 Function in the Global Stress Response Pathway in Baker's Yeast

Genetics ◽  
1996 ◽  
Vol 142 (4) ◽  
pp. 1083-1093 ◽  
Author(s):  
Carlos C Evangelista ◽  
Ana M Rodriguez Torres ◽  
M Paullin Limbach ◽  
Richard S Zitomer
Keyword(s):  
Stress Response ◽  
Heat Shock ◽  
Osmotic Stress ◽  
Regulatory Element ◽  
Regulatory Region ◽  
Mitogen Activated Protein Kinase ◽  
Regulatory Subunit ◽  
Temperature Sensitive ◽  
Global Stress ◽  
Rna Accumulation

Abstract Yeast respond to a variety of stresses through a global stress response that is mediated by a number of signal transduction pathways and the cis-acting STRE DNA sequence. The CYC7 gene, encoding iso-2-cytochrome c, has been demonstrated to respond to heat shock, glucose starvation, approach-to-stationary phase, and, as we demonstrate here, to osmotic stress. This response was delayed in a the hogl-Δ1 strain implicating the Hog1 mitogen-activated protein kinase cascade, a known component of the global stress response. Deletion analysis of the CYC7 regulatory region suggested that three STRE elements were each capable of inducing the stress response. Mutations in the ROX3 gene prevented CYC7 RNA accumulation during heat shock and osmotic stress. ROX3 RNA levels were shown to be induced by stress through a novel regulatory element. A selection for high-copy suppressors of a ROX3 temperature-sensitive allele resulted in the isolation of RTS1, encoding a protein with homology to the B′ regulatory subunit of protein phosphatase 2A0. Deletion of RTS1 caused temperature and osmotic sensitivity and increased accumulation of CYC7 RNA under all conditions. Over-expression of this gene caused increased CYC7 RNA accumulation in rox3 mutants but not in wild-type cells.

scholarly journals Genome-wide identification and analysis of the heat shock transcription factor family in moso bamboo (Phyllostachys edulis)

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bin Huang ◽  
Zhinuo Huang ◽  
Ruifang Ma ◽  
Jialu Chen ◽  
Zhijun Zhang ◽  
...  
Keyword(s):  
Heat Stress ◽  
Stress Response ◽  
Heat Shock ◽  
Gene Family ◽  
Regulatory Elements ◽  
Moso Bamboo ◽  
Naphthalene Acetic Acid ◽  
Plant Responses ◽  
Heat Stress Response ◽  
Regulatory Pathways

AbstractHeat shock transcription factors (HSFs) are central elements in the regulatory network that controls plant heat stress response. They are involved in multiple transcriptional regulatory pathways and play important roles in heat stress signaling and responses to a variety of other stresses. We identified 41 members of the HSF gene family in moso bamboo, which were distributed non-uniformly across its 19 chromosomes. Phylogenetic analysis showed that the moso bamboo HSF genes could be divided into three major subfamilies; HSFs from the same subfamily shared relatively conserved gene structures and sequences and encoded similar amino acids. All HSF genes contained HSF signature domains. Subcellular localization prediction indicated that about 80% of the HSF proteins were located in the nucleus, consistent with the results of GO enrichment analysis. A large number of stress response–associated cis-regulatory elements were identified in the HSF upstream promoter sequences. Synteny analysis indicated that the HSFs in the moso bamboo genome had greater collinearity with those of rice and maize than with those of Arabidopsis and pepper. Numerous segmental duplicates were found in the moso bamboo HSF gene family. Transcriptome data indicated that the expression of a number of PeHsfs differed in response to exogenous gibberellin (GA) and naphthalene acetic acid (NAA). A number of HSF genes were highly expressed in the panicles and in young shoots, suggesting that they may have functions in reproductive growth and the early development of rapidly-growing shoots. This study provides fundamental information on members of the bamboo HSF gene family and lays a foundation for further study of their biological functions in the regulation of plant responses to adversity.

scholarly journals TOR and RAS pathways regulate desiccation tolerance inSaccharomyces cerevisiae

2013 ◽  
Vol 24 (2) ◽  
pp. 115-128 ◽  
Author(s):  
Aaron Z. Welch ◽  
Patrick A. Gibney ◽  
David Botstein ◽  
Douglas E. Koshland
Keyword(s):  
Growth Rate ◽  
Stress Response ◽  
Heat Shock ◽  
Desiccation Tolerance ◽  
Ribosome Biogenesis ◽  
Inverse Correlation ◽  
Fold Increase ◽  
Nutrient Deprivation ◽  
Camp Pathway ◽  
Dividing Cells

Tolerance to desiccation in cultures of Saccharomyces cerevisiae is inducible; only one in a million cells from an exponential culture survive desiccation compared with one in five cells in stationary phase. Here we exploit the desiccation sensitivity of exponentially dividing cells to understand the stresses imposed by desiccation and their stress response pathways. We found that induction of desiccation tolerance is cell autonomous and that there is an inverse correlation between desiccation tolerance and growth rate in glucose-, ammonia-, or phosphate-limited continuous cultures. A transient heat shock induces a 5000–fold increase in desiccation tolerance, whereas hyper-ionic, -reductive, -oxidative, or -osmotic stress induced much less. Furthermore, we provide evidence that the Sch9p-regulated branch of the TOR and Ras-cAMP pathway inhibits desiccation tolerance by inhibiting the stress response transcription factors Gis1p, Msn2p, and Msn4p and by activating Sfp1p, a ribosome biogenesis transcription factor. Among 41 mutants defective in ribosome biogenesis, a subset defective in 60S showed a dramatic increase in desiccation tolerance independent of growth rate. We suggest that reduction of a specific intermediate in 60S biogenesis, resulting from conditions such as heat shock and nutrient deprivation, increases desiccation tolerance.

scholarly journals Impaired Temperature Stress Response of a Streptococcus thermophilus deoD Mutant

2003 ◽  
Vol 69 (2) ◽  
pp. 1287-1289 ◽  
Author(s):  
Mario Varcamonti ◽  
Maria R. Graziano ◽  
Romilde Pezzopane ◽  
Gino Naclerio ◽  
Slavica Arsenijevic ◽  
...  
Keyword(s):  
Growth Rate ◽  
Stress Response ◽  
Heat Shock ◽  
Temperature Stress ◽  
Streptococcus Thermophilus ◽  
Wild Type ◽  
Temperature Shock ◽  
Dual Response ◽  
Survival Capacity

ABSTRACT An insertional deoD mutant of Streptococcus thermophilus strain SFi39 had a reduced growth rate at 20°C and an enhanced survival capacity to heat shock compared to the wild type, indicating that the deoD product is involved in temperature shock adaptation. We report evidence that ppGpp is implicated in this dual response.

Identification of cis and trans components of a novel heat shock stress regulatory pathway in Saccharomyces cerevisiae

1993 ◽  
Vol 13 (1) ◽  
pp. 248-256
Author(s):  
N Kobayashi ◽  
K McEntee
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Stress Response ◽  
Heat Shock ◽  
Reporter Gene ◽  
Heat Shock Element ◽  
Cis Acting ◽  
Heat Shock Stress ◽  
Specific Complex ◽  
Cis And Trans ◽  
Shock Stress

The stress-responsive DDR2 gene (previously called DDRA2) of Saccharomyces cerevisiae is transcribed at elevated levels following stress caused by heat shock or DNA damage. Previously, we identified a 51-bp promoter fragment, oligo31/32, which conferred heat shock inducibility on the heterologous CYC1-lacZ reporter gene in S. cerevisiae (N. Kobayashi and K. McEntee, Proc. Natl. Acad. Sci. USA 87:6550-6554, 1990). Using a series of synthetic oligonucleotides, we have identified a pentanucleotide, CCCCT (C4T), as an essential component of this stress response sequence. This element is not a binding site for the well-characterized heat shock transcription factor which recognizes a distinct cis-acting heat shock element in the promoters of many heat shock genes. Here we demonstrate the ability of oligonucleotides containing the C4T sequence to confer heat shock inducibility on the reporter gene and show that the presence of two such elements produces more than additive effects on induction. Gel retardation experiments have been used to demonstrate specific complex formation between C4T-containing fragments and one or more yeast proteins. Formation of these complexes was not competed by fragments containing mutations in the C4T sequence nor by heat shock element-containing competitor DNAs. Fragments containing the C4T element bound to a single 140-kDa polypeptide, distinct from heat shock transcription factors in yeast crude extracts. These experiments identify key cis- and trans-acting components of a novel heat shock stress response pathway in S. cerevisiae.

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