Neuronal HSF-1 coordinates the propagation of fat desaturation across tissues to enable adaptation to high temperatures in C. elegans
Creators
- Chauve, Laetitia1
- Hodge, Francesca1
- Murdoch, Sharlene1
- Masoudzadeh, Fatemah1
- Mann, Harry-Jack1
- Lopez-Clavijo, Andrea1
- Okkenhaug, Hanneke1
- West, Greg1
- Sousa, Bebiana C.1
- Segonds-Pichon, Anne1
- Li, Cheryl1
- Wingett, Steven1
- Kienberger, Hermine2
- Kleigrewe, Karin2
- De Bono, Mario3
- Wakelam, Michael1
- Casanueva, Olivia1
- 1. Babraham Institute
- 2. Bavarian Centre for Biomolecular mass spectrometry, Freising, Germany
- 3. Institute of Science and Technology, Klosterneuburg, Austria
Description
To survive elevated temperatures, ectotherms adjust the fluidity of membranes by fine-tuning lipid desaturation levels in a process previously described to be cell-autonomous. We have discovered that, in Caenorhabditis elegans, neuronal Heat shock Factor 1 (HSF-1), the conserved master regulator of the heat shock response (HSR)- causes extensive fat remodelling in peripheral tissues. These changes include a decrease in fat desaturase and acid lipase expression in the intestine, and a global shift in the saturation levels of plasma membrane’s phospholipids. The observed remodelling of plasma membrane is in line with ectothermic adaptive responses and gives worms a cumulative advantage to warm temperatures. We have determined that at least six TAX-2/TAX-4 cGMP gated channel expressing sensory neurons and TGF-β/BMP are required for signalling across tissues to modulate fat desaturation. We also find neuronal hsf-1 is not only sufficient but also partially necessary to control the fat remodelling response and for survival at warm temperatures. This is the first study to show that a thermostat-based mechanism can cell non-autonomously coordinate membrane saturation and composition across tissues in a multicellular animal.
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