Predator-secreted sulfolipids induce defensive responses in C. elegans

Zheng Liu, Maro J. Kariya, Christopher D. Chute, Amy K. Pribadi, Sarah G. Leinwand, Ada Tong, Kevin P. Curran, Neelanjan Bose, Frank C. Schroeder, Jagan Srinivasan and Sreekanth H. Chalasani ()
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Zheng Liu: The Salk Institute for Biological Studies
Maro J. Kariya: Cornell University
Christopher D. Chute: Worcester Polytechnic Institute
Amy K. Pribadi: The Salk Institute for Biological Studies
Sarah G. Leinwand: The Salk Institute for Biological Studies
Ada Tong: The Salk Institute for Biological Studies
Kevin P. Curran: The Salk Institute for Biological Studies
Neelanjan Bose: Cornell University
Frank C. Schroeder: Cornell University
Jagan Srinivasan: Worcester Polytechnic Institute
Sreekanth H. Chalasani: The Salk Institute for Biological Studies

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract Animals respond to predators by altering their behavior and physiological states, but the underlying signaling mechanisms are poorly understood. Using the interactions between Caenorhabditis elegans and its predator, Pristionchus pacificus, we show that neuronal perception by C. elegans of a predator-specific molecular signature induces instantaneous escape behavior and a prolonged reduction in oviposition. Chemical analysis revealed this predator-specific signature to consist of a class of sulfolipids, produced by a biochemical pathway required for developing predacious behavior and specifically induced by starvation. These sulfolipids are detected by four pairs of C. elegans amphid sensory neurons that act redundantly and recruit cyclic nucleotide-gated (CNG) or transient receptor potential (TRP) channels to drive both escape and reduced oviposition. Functional homology of the delineated signaling pathways and abolishment of predator-evoked C. elegans responses by the anti-anxiety drug sertraline suggests a likely conserved or convergent strategy for managing predator threats.

Date: 2018
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DOI: 10.1038/s41467-018-03333-6

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