(Submitter supplied) 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-β/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.
- Organism:
- Caenorhabditis elegans
- Type:
- Expression profiling by high throughput sequencing
- Platform:
- GPL18245
- 6 Samples
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