Faculty Opinions recommendation of Regulation of the cellular heat shock response in Caenorhabditis elegans by thermosensory neurons.

2008 ◽  
Author(s):  
Nektarios Tavernarakis
Keyword(s):  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Shock Response

scholarly journals A novel assay for drug screening that utilizes the heat shock response of Caenorhabditis elegans nematodes

PLoS ONE ◽  
2020 ◽  
Vol 15 (10) ◽  
pp. e0240255
Author(s):  
Chih-Hsiung Chen ◽  
Rahul Patel ◽  
Alessandro Bortolami ◽  
Federico Sesti
Keyword(s):  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Drug Screening ◽  
Heat Shock Response ◽  
Shock Response

scholarly journals Dynamics of Heat Shock Detection and Response in the Intestine of Caenorhabditis elegans

2019 ◽  
Author(s):  
Erin K. Dahlstrom ◽  
Erel Levine
Keyword(s):  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Protein Misfolding ◽  
Single Cells ◽  
Molecular Response ◽  
Longitudinal Measurements ◽  
Cell Tissue ◽  
Shock Response ◽  
Protein Misfolding And Aggregation

AbstractThe heat shock response is the organized molecular response to stressors which disrupt proteostasis, potentially leading to protein misfolding and aggregation. While the regulation of the heat shock response is well-studied in single cells, its coordination at the cell, tissue, and systemic levels of a multicellular organism is poorly understood. To probe the interplay between systemic and cell-autonomous responses, we studied the upregulation of HSP-16.2, a molecular chaperone induced throughout the intestine of Caenorhabditis elegans following a heat shock, by taking longitudinal measurements in a microfluidic environment. Based on the dynamics of HSP-16.2 accumulation, we showed that a combination of heat shock temperature and duration define the intensity of stress inflicted on the worm and identified two regimes of low and high intensity stress. Modeling the underlying regulatory dynamics implicated the saturation of heat shock protein mRNA production in defining these two regimes and emphasized the importance of time separation between transcription and translation in establishing these dynamics. By applying a heat shock and measuring the response in separate parts of the animals, we implicated thermosensory neurons in accelerating the response and transducing information within the animal. We discuss possible implications of the systemic and cell level aspects and how they coordinate to facilitate the organismal response.

scholarly journals Systemic activation coordinates the heat shock response of the insulin/IGF-1 pathway in Caenorhabditis elegans

2017 ◽  
Author(s):  
Ronen B Kopito ◽  
Kathie Watkins ◽  
Erel Levine
Keyword(s):  
Caenorhabditis Elegans ◽  
Stress Response ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Cellular Response ◽  
Precise Control ◽  
Cellular Processes ◽  
Shock Response ◽  
Stressed Cells ◽  
Shock Proteins

Exposure to high temperatures has an adverse effect on cellular processes and results in activation of the cellular heat shock response (HSR), a highly conserved program of inducible genes to maintain protein homeostasis1. The insulin/IGF-1 signaling (IIS) pathway, which has diverse roles from metabolism to stress response and longevity, is activated as part of the HSR2–4. Recent evidence suggest that the IIS pathway is able to affect proteostasis non-autonomously5,6, yet it is not known if it is activated autonomously in stressed cells or systemically as part of an organismic program. In Caenorhabditis elegans, the single forkhead box O (FOXO) homologue DAF-16 functions as the major target of the IIS pathway7 and, together with the heat-shock factor HSF-1, induce the expression of small heat shock proteins in response to heat shock8–10,3. Here we use a novel microfluidic device that allows precise control of the spatiotemporal temperature profile to show that cellular activation of DAF-16 integrates local temperature sensation with systemic signals. We demonstrate that DAF-16 activation in head sensory neurons is essential for DAF-16 activation in other tissues, but show that no known thermosensory neuron is individually required. Our findings demonstrate that systemic and cell-autonomous aspects of stress response act together to facilitate a coordinated cellular response at the organismic level.

scholarly journals Caenorhabditis elegans AF4/FMR2 Family Homolog affl-2 Regulates Heat-Shock-Induced Gene Expression

Genetics ◽  
2020 ◽  
Vol 215 (4) ◽  
pp. 1039-1054
Author(s):  
Sophie J. Walton ◽  
Han Wang ◽  
Porfirio Quintero-Cadena ◽  
Alex Bateman ◽  
Paul W. Sternberg
Keyword(s):  
Gene Expression ◽  
Heat Stress ◽  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Genetic Locus ◽  
Transcriptional Response ◽  
Transcriptional Elongation ◽  
Link Type ◽  
Shock Response

To mitigate the deleterious effects of temperature increases on cellular organization and proteotoxicity, organisms have developed mechanisms to respond to heat stress. In eukaryotes, HSF1 is the master regulator of the heat shock transcriptional response, but the heat shock response pathway is not yet fully understood. From a forward genetic screen for suppressors of heat-shock-induced gene expression in Caenorhabditis elegans, we found a new allele of hsf-1 that alters its DNA-binding domain, and we found three additional alleles of sup-45, a previously molecularly uncharacterized genetic locus. We identified sup-45 as one of the two hitherto unknown C. elegans orthologs of the human AF4/FMR2 family proteins, which are involved in regulation of transcriptional elongation rate. We thus renamed sup-45 as affl-2 (AF4/FMR2-Like). Through RNA-seq, we demonstrated that affl-2 mutants are deficient in heat-shock-induced transcription. Additionally, affl-2 mutants have herniated intestines, while worms lacking its sole paralog (affl-1) appear wild type. AFFL-2 is a broadly expressed nuclear protein, and nuclear localization of AFFL-2 is necessary for its role in heat shock response. affl-2 and its paralog are not essential for proper HSF-1 expression and localization after heat shock, which suggests that affl-2 may function downstream of, or parallel to, hsf-1. Our characterization of affl-2 provides insights into the regulation of heat-shock-induced gene expression to protect against heat stress.

scholarly journals CCAR-1 is a negative regulator of the heat-shock response in Caenorhabditis elegans

Aging Cell ◽  
2018 ◽  
Vol 17 (5) ◽  
pp. e12813 ◽  
Author(s):  
Jessica Brunquell ◽  
Rachel Raynes ◽  
Philip Bowers ◽  
Stephanie Morris ◽  
Alana Snyder ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Negative Regulator ◽  
Shock Response
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