Neuronal HSF-1 coordinates the propagation of fat desaturation across tissues to enable adaptation to high temperatures in < i > C < /i > . < i > elegans < /i >

by Laetitia Chauve, Francesca Hodge, Sharlene Murdoch, Fatemah Masoudzadeh, Harry-Jack Mann, Andrea Lopez-Clavijo, Hanneke Okkenhaug, Greg West, Bebiana C. Sousa, Anne Segonds-Pichon, Cheryl Li, Steven Wingett, Hermine Kienberger, Karin Kleigrewe, Mario De Bono, Michael Wakelam, Olivia Casanueva

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, inCaenorhabditis elegans, neuronal heat shock factor 1 (HSF-1), the conserved master regulator of the heat shock response (HSR), causes extensive fat remodeling 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 remodeling 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 6 TAX-2/TAX-4 cyclic guanosine monophosphate (cGMP) gated channel expressing sensory neurons, an d transforming growth factor ß (TGF-β)/bone morphogenetic protein (BMP) are required for signaling across tissues to modulate fat desaturation. We also find neuronalhsf-1 is not only sufficient but also partially necessary to control the fat remodeling response and for survival at warm temperatures. This is the first study to show that a thermostat-based...

Source: PLoS Biology: Archived Table of Contents - November 1, 2021 Category: Biology Authors: Laetitia Chauve Source Type: research