FLP-15 modulates the amplitude of body-bends during locomotion in Caenorhabditis elegans.

Locomotion is essential for executing most behaviours. In Caenorhabditis elegans, efficient locomotion is exhibited as a result of the coordination of excitatory and inhibitory signals from the nervous system onto the body-wall muscles. Although neurotransmitters play a vital role in maintaining and executing coordinated movements, neuropeptides have emerged as important players in the regulation and sustenance of locomotory states. In this study we show that mutants in the neuropeptide flp-15 show a large increase in the mean amplitude of body-bends, indicating defects in the locomotory state of these animals. Our data suggest that FLP-15 partially functions through the G-protein coupled receptor (GPCR) NPR-3 to regulate the amplitude of body-bends. Finally, we show that loss of flp-15 leads to an increase in the expression of another neuropeptide, NLP-12, whose over-expression has been implicated in causing increased amplitude of body-bends, allowing us to speculate that the regulation of NLP-12 by FLP-15 may allow for the observed locomotory defects in flp-15 mutant animals.