Co-regulation of cold-resistant food acquisition by insulin- and neuropeptide Y-like systems in Drosophila melanogaster.

To survive, food-deprived animals may be forced to forage under hostile conditions. We attempt to use genetically tractable Drosophila melanogaster as a model to elucidate molecular and neural mechanisms that drive a forager to engage in risk-prone food acquisition. Here we describe a paradigm for assessing hunger-driven food acquisition by fly larvae at a deleteriously cold temperature. Genetic analyses reveal that the neural activity of NPFR1, a receptor of neuropeptide F (NPF, the sole fly homolog of neuropeptide Y or NPY), was required for cold-resistant feeding behavior of fasted larvae. Conversely, NPFR1 overexpression in fed larvae was sufficient to trigger cold-resistant feeding activity normally associated with fasted larvae. Furthermore, the fly insulin-like system, implicated in the transduction of hunger signals to the CNS, regulated negatively larval cold-resistant food acquisition. The results from this and our previous studies suggest that the fly NPY-like system is a central mediator of hunger-elicited resistance to diverse stressors that can be of thermal, gustatory or mechanical form.