In C.elegans , starvation is known to alter several behaviors, including olfactory adaptation and feeding. Feeding-defective mutants can be useful tools to analyze behaviors affected by starvation. We have been analyzing locomotory activity of eat mutants. We have identified a novel eat locus,
eat-20 , by a reverse genetic approach. In
eat-20 mutants, the pharyngeal pumping rate was slowed and bacterial transport was inefficient, and the mutants exhibited the starved appearance typical of eat mutants. We have noticed that
eat-20 mutants were hyperactive in locomotion. Most of previously identified eat mutants, such as
eat-2, 4, 10, 11, 13 and 15 , were also hyperactive in the presence of food. The extent of increase of the locomotory activity generally correlated with the strength of Eat phenotype of the mutants. These results suggest that hyperactivity is caused by feeding defects. Octopamine was reported to have effects that were similar to those of the depletion of food on several behaviors of worms. We have revealed that exogenous octopamine, in the presence of food, enhanced the activity of wild type animals to the level similar to that of strong Eat mutants. Octopamine did not further enhance the activity of strong Eat mutants. Phentolamine, which is known to block an octopamine receptor in the locust, did not affect the activity of wild type worms in the presence of food, but decreased the activity of eat mutants to the level of untreated wild type animals. We propose a model that , in eat mutants, starvation promotes the release of octopamine which in turn activates a neural pathway controlling locomotion. Together with the previously reported observations, our results suggest that octopamine transmits a starvation signal in C.elegans .