RT Journal Article SR Electronic T1 A neuronal thermostat controls membrane fluidity in C. elegans JF bioRxiv FD Cold Spring Harbor Laboratory SP 2019.12.20.882514 DO 10.1101/2019.12.20.882514 A1 L Chauve A1 S Murdoch A1 F. Masoudzadeh A1 F. Hodge A1 A. Lopez-Clavijo A1 H. Okkenhaug A1 G. West A1 A. Segonds-Pichon A1 S. Wingett A1 M. Wakelam A1 K. Kienberger A1 K. Kleigrewe A1 O Casanueva YR 2019 UL http://biorxiv.org/content/early/2019/12/24/2019.12.20.882514.abstract AB An organisms’ ability to adapt to heat can be key to its survival. Cells adapt to temperature shifts by adjusting lipid desaturation levels and the fluidity of membranes in a process that is thought to be controlled cell autonomously. We have discovered that subtle, step-wise increments in ambient temperature can lead to the conserved heat shock response being activated in head neurons of C. elegans. This response is exactly opposite to the expression of the lipid desaturase FAT-7 in the worm’s gut. We find that the over-expression of the master regulator of this response, Hsf-1, in head neurons, causes extensive fat remodeling to occur across tissues. These changes include a decrease in FAT-7 expression and a shift in the levels of unsaturated fatty acids in the plasma membrane. These shifts are in line with membrane fluidity requirements to survive in warmer temperatures. We have identified that the cGMP receptor, TAX-2/TAX-4, as well as TGF-β/BMP signaling, as key players in the transmission of neuronal stress to peripheral tissues. This is the first study to suggest that a thermostat-based mechanism can centrally coordinate membrane fluidity in response to warm temperatures across tissues in multicellular animals.