Neuronal HSF-1 activity coordinates fat desaturation across tissues in C. elegans via TGF-b/BMP signalling

To survive elevated temperatures, ectotherms adjust the fluidity of membranes by fine-tuning lipid desaturation levels in a process that has been previously described to be cell-autonomous. We have discovered that, in Caenorhabditis elegans, the neuronal over-expression of the master regulator of the conserved heat shock response (HSR), Hsf-1, causes extensive fat remodelling in peripheral tissues. These changes include a decrease in fat desaturase expression in the gut, and a shift in the saturation levels of fatty acids in the plasma membrane, in line with ectothermic adaptive responses. We have identified the cGMP receptor TAX-2/TAX-4 and TGF-ß/BMP signalling, as key players in signalling across tissues. We also find that gradual increments in ambient temperature result in HSR activation exclusively in wild-type head neurons. This is the first study to suggest that a thermostat-based mechanism can non-cell autonomously coordinate membrane fluidity in response to warm temperatures across tissues in multicellular animals. Overall design: RNA-seq comparison between young adult N2 (WT) and AGD1289 (neuronal over-expression of HSF-1)