Glia of <i>C. elegans</i> coordinate a protective organismal heat shock response independent of the neuronal thermosensory circuit.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 36490338.
- Also identified by DOI 10.1126/sciadv.abq3970 and PMC identifier 9733925.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Aging organisms lose the ability to induce stress responses, becoming vulnerable to protein toxicity and tissue damage. Neurons can signal to peripheral tissues to induce protective organelle-specific stress responses. Recent work shows that glia can independently induce such responses. Here, we show that overexpression of heat shock factor 1 (<i>hsf-1</i>) in the four astrocyte-like cephalic sheath cells of <i>Caenorhabditis elegans</i> induces a non-cell-autonomous cytosolic unfolded protein response, also known as the heat shock response (HSR). These animals have increased lifespan and heat stress resistance and decreased protein aggregation. Glial HSR regulation is independent of canonical thermosensory circuitry and known neurotransmitters but requires the small clear vesicle release protein UNC-13. HSF-1 and the FOXO transcription factor DAF-16 are partially required in peripheral tissues for non-cell-autonomous HSR, longevity, and thermotolerance. Cephalic sheath glial <i>hsf-1</i> overexpression also leads to pathogen resistance, suggesting a role for this signaling pathway in immune function.