The cellular stress response and temperature: Function, regulation, and evolution

Somero, George N.

doi:10.1002/jez.2344

Cited by 151 publications

(114 citation statements)

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“…The mechanistic basis of the different responses to 25, 30 and 35°C was not examined, but the different responses among these three groups may reflect the extent of cellular damage caused by the three sublethal heat-stress temperatures and, thus, the extent to which the cellular stress response (CSR) was activated [43,44]. Studies of the effects of field body temperature on gene expression in M. californianus have shown a strong temperature-dependence of the expression of stressrelated genes, e.g.…”

Section: Discussionmentioning

confidence: 99%

A single heat-stress bout induces rapid and prolonged heat acclimation in the California mussel,Mytilus californianus

et al. 2020

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Climate change is not only causing steady increases in average global temperatures but also increasing the frequency with which extreme heating events occur. These extreme events may be pivotal in determining the ability of organisms to persist in their current habitats. Thus, it is important to understand how quickly an organism's heat tolerance can be gained and lost relative to the frequency with which extreme heating events occur in the field. We show that the California mussel, Mytilus californianus —a sessile intertidal species that experiences extreme temperature fluctuations and cannot behaviourally thermoregulate—can quickly (in 24–48 h) acquire improved heat tolerance after exposure to a single sublethal heat-stress bout (2 h at 30 or 35°C) and then maintain this improved tolerance for up to three weeks without further exposure to elevated temperatures. This adaptive response improved survival rates by approximately 75% under extreme heat-stress bouts (2 h at 40°C). To interpret these laboratory findings in an ecological context, we evaluated 4 years of mussel body temperatures recorded in the field. The majority (approx. 64%) of consecutive heat-stress bouts were separated by 24–48 h, but several consecutive heat bouts were separated by as much as 22 days. Thus, the ability of M. californianus to maintain improved heat tolerance for up to three weeks after a single sublethal heat-stress bout significantly improves their probability of survival, as approximately 33% of consecutive heat events are separated by 3–22 days. As a sessile animal, mussels likely evolved the capability to rapidly gain and slowly lose heat tolerance to survive the intermittent, and often unpredictable, heat events in the intertidal zone. This adaptive strategy will likely prove beneficial under the extreme heat events predicted with climate change.

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Section: Discussionmentioning

confidence: 99%

A single heat-stress bout induces rapid and prolonged heat acclimation in the California mussel,Mytilus californianus

et al. 2020

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“…In organisms or the cells, thermal stress may exert effects on multiple signaling pathways [49][50][51], but we focused on the TRPV2-related pathways. We found that at least 3 pathways were activated during the overactivation of TRPV2, including HSPs (HSP70, HSP27), TNFα and PI3K pathways.…”

Section: Discussionmentioning

confidence: 99%

Thermal stress involved in TRPV2 promotes tumorigenesis through the pathway of PI3K/Akt/mTOR in esophageal squamous cell carcinoma

Huang¹,

Li²,

Tian³

et al. 2020

Preprint

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BackgroundEsophageal squamous cell carcinoma (ESCC) is a leading cause of cancer death worldwide. Although the exposure of esophageal mucosa to heat stimuli has long been recognized as an important risk for the initiation and development of ESCC, its underlying mechanisms remain uncharacterized. MethodsWestern blotting and immunofluorescence were used to detect the expression and localization of transient receptor potential vanilloid receptor 2 (TRPV2) in the ESCC cells. The cancerous behaviors of the ESCC cells were evaluated by a single-cell culturing assay, a wound healing assay, a 3D culturing assay and a tube formation assay respectively. In vivo tumorigenicity and metastasis of the ESCC cells were examined via xenograft nude mouse models. Western blotting and IHC were performed to determine the expression profiles of TRPV2 in the ESCC patient tissues. TRPV2 knocked-out ESCC cell line was established using CRISPR-Cas9 gene editing technique.ResultsHere, we found that the expression of TRPV2, one of the thermally sensitive TRP family members, was upregulated in both ESCC cells and clinical samples. We further showed that activation of TRPV2 by recurrent acute thermal stress (54°C, a temperature unexpectedly much lower than those in many dietary modalities) or O1821 (20 μM), a TRPV2 agonist, promoted cancerous behaviors in ESCC cells. The proangiogenic capacity of the heat-challenged ESCC cells was also found to be enhanced profoundly in the tube formation assay; both tumor formation and metastasis that originated from the cells were substantially promoted in nude mouse models upon the activation of TRPV2. These effects were inhibited significantly by tranilast (120 μM), a TRPV2 inhibitor, and abolished by TRPV2 knock-out using CRISPR-Cas9 gene editing. Conversely, overexpression of TRPV2 by transfection of TRPV2 DNA into NE2 cells, could switch the cells to tumorigenesis upon activation of TRPV2. Mechanistically, the driving role of TRPV2 in the progression of ESCC is mainly regulated by the PI3K/Akt/mTOR signaling pathway. Application of a pan-PI3K/mTOR inhibitor and/or a PTEN activator resulted in markedly reduced ESCC cell proliferation. ConclusionsOur study first proved that TRPV2 plays an important role in the tumorigenesis of ESCC upon thermal stress. We revealed that TRPV2-PI3K/Akt/mTOR is a novel and promising target for the prevention and treatment of ESCC.

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“…For example, molecular sliding clamps routinely monitor rates of DNA damage and activate DNA repair and other CSR mechanisms when DNA damage exceeds the homeostatic range (Freeman & Monteiro, 2010). Another example are molecular chaperones that monitor rates of protein unfolding by proportional release of sequestered CSR transcription factors, a mechanism known as the heat shock response (Somero, 2020). Thus, macromolecular damage exacerbates system dysregulation and controls CSR activation.…”

Section: The Elastic Limit and Breaking Point Of Biological Systemsmentioning

confidence: 99%

Defining biological stress and stress responses based on principles of physics

Kültz

2020

J Exp Zool Pt A

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Stress represents a multi-faceted force that is central for the evolution of life. Organisms evolve while adapting to stress and stressful contexts often represent selective bottlenecks. To understand stress effects on biological systems and corresponding coping strategies it is imperative to properly define stress and the resulting strain that triggers compensatory responses in cells and organisms. Here I am deriving such definitions for biological systems based on principles that are established in physics. The relationship between homeostasis of critical biological variables, the elastic limit, the cellular stress response (CSR), cellular homeostasis response (CHR), system dysregulation, and the breaking point (death of the system) is outlined. Dysregulation of homeostatic set-points of biological variables perturbs the functional properties of the system, shifting them out of the evolutionarily optimized range. Such shifts are accompanied by elevated rates of macromolecular damage, which represents a non-specific signal for induction of a universal response, the CSR. The CSR complements the CHR in re-establishing homeostasis of the system as a whole. Moreover, the CSR is essential for coping with suboptimal conditions while the system is in a dysregulated state and for removing excessive damage that accumulates during such periods. The extreme complexity of biological systems and their emergent properties often necessitate monitoring stress effects on many biological variables simultaneously to properly deduce stress effects on the system as a whole. Therefore, increased utilization of systems biology (omics) This is the author manuscript accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as

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The cellular stress response and temperature: Function, regulation, and evolution

Cited by 151 publications

References 84 publications

A single heat-stress bout induces rapid and prolonged heat acclimation in the California mussel,Mytilus californianus

A single heat-stress bout induces rapid and prolonged heat acclimation in the California mussel,Mytilus californianus

Thermal stress involved in TRPV2 promotes tumorigenesis through the pathway of PI3K/Akt/mTOR in esophageal squamous cell carcinoma

Defining biological stress and stress responses based on principles of physics

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