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.
Highlights
Animals respond to predators by altering their behavior and physiological states, but the underlying signaling mechanisms are poorly understood
We found that predator cue had no significant effect on C. elegans taxis responses in this assay (Supplementary Fig. S1c,d), indicating that volatiles do not contribute to the activity of predator cue
These results show that starving P. pacificus release potent non-volatile repellent(s) that induce rapid C. elegans avoidance
Summary
Animals respond to predators by altering their behavior and physiological states, but the underlying signaling mechanisms are poorly understood. In mice, the chemosensory neurons in the vomeronasal organ (VNO), Grueneberg ganglion, and main olfactory epithelium have been shown to facilitate defensive behaviors through detection of signals from cat urine and fox feces[3,7,8] These neurons project to higher brain regions where predator odor information is processed to generate stereotyped defensive behaviors[9]. The precise identities of the participating neurons, their connections, and the nature of the circuit computations driving these invariant defensive behaviors have remained elusive We approached these questions by analyzing the behavioral responses of the nematode Caenorhabditis elegans[11] to a predatory nematode Pristionchus pacificus[12]. These P. pacificus-derived chemical signals are detected by C. elegans via multiple sensory neurons and processed via conserved signaling pathways
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