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A neuronal thermostat controls membrane fluidity in C. elegans

L Chauve, S Murdoch, F. Masoudzadeh, F. Hodge, A. Lopez-Clavijo, H. Okkenhaug, G. West, A. Segonds-Pichon, S. Wingett, M. Wakelam, K. Kienberger, K. Kleigrewe, O Casanueva
doi: https://doi.org/10.1101/2019.12.20.882514
L Chauve
1Babraham Institute, Cambridge, UK
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S Murdoch
1Babraham Institute, Cambridge, UK
2Epigenetics Department
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F. Masoudzadeh
1Babraham Institute, Cambridge, UK
2Epigenetics Department
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F. Hodge
1Babraham Institute, Cambridge, UK
2Epigenetics Department
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A. Lopez-Clavijo
1Babraham Institute, Cambridge, UK
2Epigenetics Department
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H. Okkenhaug
1Babraham Institute, Cambridge, UK
2Epigenetics Department
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G. West
1Babraham Institute, Cambridge, UK
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A. Segonds-Pichon
1Babraham Institute, Cambridge, UK
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S. Wingett
1Babraham Institute, Cambridge, UK
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M. Wakelam
1Babraham Institute, Cambridge, UK
3Signalling Department
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K. Kienberger
4Bavarian Center for Biomolecular Mass Spectometry, Germany
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K. Kleigrewe
4Bavarian Center for Biomolecular Mass Spectometry, Germany
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O Casanueva
1Babraham Institute, Cambridge, UK
2Epigenetics Department
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  • For correspondence: olivia.casanueva@babraham.ac.uk
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Summary

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.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted December 24, 2019.
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A neuronal thermostat controls membrane fluidity in C. elegans
L Chauve, S Murdoch, F. Masoudzadeh, F. Hodge, A. Lopez-Clavijo, H. Okkenhaug, G. West, A. Segonds-Pichon, S. Wingett, M. Wakelam, K. Kienberger, K. Kleigrewe, O Casanueva
bioRxiv 2019.12.20.882514; doi: https://doi.org/10.1101/2019.12.20.882514
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A neuronal thermostat controls membrane fluidity in C. elegans
L Chauve, S Murdoch, F. Masoudzadeh, F. Hodge, A. Lopez-Clavijo, H. Okkenhaug, G. West, A. Segonds-Pichon, S. Wingett, M. Wakelam, K. Kienberger, K. Kleigrewe, O Casanueva
bioRxiv 2019.12.20.882514; doi: https://doi.org/10.1101/2019.12.20.882514

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