ArticleCurrent biology : CB2015
Neuronal serotonin release triggers the heat shock response in C. elegans in the absence of temperature increase.
Article in Current biology : CB, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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89 citing papers in PubMed, 150 citations in OpenAlex.
- A neuronal GPCR modifies neuropeptide signaling to suppress proteostasis in distal tissues.Science advances · 2026Article
- Light sensing enhances thermotolerance and competitive fitness via serotonergic signaling in an eyeless organism.Cell research · 2026Article
- Modulation of host proteostasis by Prevotella corporis via induction of the heat shock response.Cell stress & chaperones · 2026Article
- A J-domain protein enhances memory by promoting physiological amyloid formation inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Adaptive inter-tissue proteostasis networks in aging and neurodegeneration.Bioscience reports · 2026Review
- Deciphering the regulatory mechanism of neural behavioral decisions through biogenic amine-mediated modulation of neural circuits inFrontiers in systems neuroscience · 2026Review
- A default silencing mechanism restrains stress-induced genes inbioRxiv : the preprint server for biology · 2025Article
- Soma to neuron communication links stress adaptation to stress avoidance behavior.bioRxiv : the preprint server for biology · 2025Article
- Aversive experiences induce valence plasticity of instructive signals to change future learning rules in mice.Communications biology · 2025Article
- Methionine cycle in C. elegans serotonergic neurons regulates diet-dependent behaviour and longevity through neuron-gut signaling.Nature communications · 2025Article
- Transcriptomics of theEcology and evolution · 2025Article
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- A nucleolar mechanism suppresses organismal proteostasis by modulating TGFβ/ERK signalling.Nature cell biology · 2025Article
- Hyperthermia and targeting heat shock proteins: innovative approaches for neurodegenerative disorders and Long COVID.Frontiers in neuroscience · 2025Review
- Docosahexaenoic Acid (DHA) Supplementation in a Triglyceride Form Prevents from Polyglutamine-Induced Dysfunctions inInternational journal of molecular sciences · 2024Article
- Neuronal IL-17 controlsProceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Third Annual Symposium of the Midwest Aging Consortium.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- A short peptide protects from age-onset proteotoxicity.Aging cell · 2023Article
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- Neuronal HLH-30/TFEB modulates peripheral mitochondrial fragmentation to improve thermoresistance in Caenorhabditis elegans.Aging cell · 2023Article
29 more citing papers are in PubMed but not listed here.
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8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundCellular mechanisms aimed at repairing protein damage and maintaining homeostasis, widely understood to be triggered by the damage itself, have recently been shown to be under cell nonautonomous control in the metazoan C. elegans. The heat shock response (HSR) is one such conserved mechanism, activated by cells upon exposure to proteotoxic conditions such as heat. Previously, we had shown that this conserved cytoprotective response is regulated by the thermosensory neuronal circuitry of C. elegans. Here, we investigate the mechanisms and physiological relevance of neuronal control.
resultsBy combining optogenetic methods with live visualization of the dynamics of the heat shock transcription factor (HSF1), we show that excitation of the AFD thermosensory neurons is sufficient to activate HSF1 in another cell, even in the absence of temperature increase. Excitation of the AFD thermosensory neurons enhances serotonin release. Serotonin release elicited by direct optogenetic stimulation of serotonergic neurons activates HSF1 and upregulates molecular chaperones through the metabotropic serotonin receptor SER-1. Consequently, excitation of serotonergic neurons alone can suppress protein misfolding in C. elegans peripheral tissue.
conclusionsThese studies imply that thermosensory activity coupled to serotonergic signaling is sufficient to activate the protective HSR prior to frank proteotoxic damage. The ability of neurosensory release of serotonin to control cellular stress responses and activate HSF1 has powerful implications for the treatment of protein conformation diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.