Oxytocin has a conserved role in regulating animal social behaviour including parental-offspring interactions. Recently an oxytocin-like neuropeptide, nematocin, and its cognate receptors have been identified in the nematode Caenorhabditis elegans. We provide evidence for a pheromone signal produced by C. elegans larvae that modifies the behaviour of adult animals in an oxytocin-dependent manner increasing their probability of leaving a food patch which the larvae are populating. This increase is positively correlated to the size of the larval population but cannot be explained by food depletion nor is it modulated by biogenic amines, which suggest it is not an aversive behaviour. Moreover, the food-leaving behaviour is conspecific and pheromone dependent: C. elegans adults respond more strongly to C. elegans larvae compared to other nematode species and this effect is absent in C. elegans daf-22 larvae which are pheromone deficient. Neurotransmitter receptors previously implicated in C. elegans foraging decisions NPR-1 and TYRA-3, for NPY-like neuropeptides and tyramine respectively, do not appear to be involved in oxytocin-dependent adult food-leaving. We conclude oxytocin signals within a novel neural circuit that regulates parental-offspring social behaviour in C. elegans and that this provides evidence for evolutionary conservation of molecular components of a parental decision making behaviour.
In its native environment of rotting vegetation, the soil nematode Caenorhabditis elegans encounters a range of bacteria. This includes species from the ESKAPE group of pathogens that pose a clinical problem in acquired hospital infections. Here, we investigated three Gram-negative members of the ESKAPE group, Pseudomonas aeruginosa, Klebsiella pneumoniae, and Acinetobacter baumannii. Pathogenicity profiles as measured by time to kill adult C. elegans showed that P. aeruginosa was the most pathogenic, followed by K. pneumoniae, while C. elegans cultured on A. baumannii exhibited the same survival as those on the standard laboratory food source for C. elegans, Escherichia coli OP50. The pathogenicity was paralleled by a reduction in time that C. elegans resided on the bacterial lawn with the most pathogenic strains triggering an increase in the frequency of food-leaving. Previous reports indicate that gut colonization is a feature of pathogenicity, but we found that the most pathogenic strains were not associated with the highest level of colonization. Indeed, clearance of P. aeruginosa strains from the C. elegans gut was independent of bacterial pathogenicity. We show that this clearance is regulated by neuromodulation as C. elegans mutants in unc-31 and egl-3 have enhanced clearance of P. aeruginosa. Intriguingly this is also not linked to their pathogenicity. It is likely that there is a dynamic balance occurring in the C. elegans intestinal environment between maintaining a healthy, beneficial microbiota and removal of pathogenic bacteria.
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