Egg-laying in C. elegans is regulated by sensory cues. For instance, it has been found that food deprivation increases the length of the inactive phase of egg-laying. However, the exact mechanisms by which this occurs are not known. We are investigating this phenomenon by focussing on two pathways, the
flp-1 pathway and the type II TGF-beta dauer pathway. The gene
flp-1 encodes a precursor of FMRFamide related neuropeptides, and it was shown by Chris Li to be expressed in a specific subset of head neurons. She found that
flp-1 knockouts affect a variety of behaviors, including egg-laying. When we tested
flp-1 worms, we found that they had a lengthened inactive phase (similar to the food-deprived worms). In addition, their egg-laying rate did not change depending on the presence or absence of food. Ablation experiments have shown that the effects of
flp-1 encoded peptides on egg-laying are independent of the presence of the HSN. Thus, we believe that the effects of FLP-1 may be mediated, at least in part, by a hormonal mechanism. Jim Thomas' lab showed that the type II TGF-beta daf (dauer formation) mutants also displayed defects in egg-laying. As the Ruvkun and Riddle labs found that the TGF-beta pathway functions in sensory neurons, it seems to be a reasonable candidate to be involved in the regulation of egg-laying by sensory cues. Interestingly, we found that the egg-laying patterns of the Daf-c mutants (
daf-1,
daf-4,
daf-7, and
daf-8) are similar to that of
flp-1: all have a lengthened inactive period of egg-laying. In addition, the egg-laying of
daf-4 and
daf-8 (but not
daf-1 or
daf-7) is unable to be modulated by the presence or absence of food. Furthermore, we found that the Daf-d mutation in
daf-3 does not cause a defect in food modulation, and in fact has the ability to suppress the food insensitivity of
daf-4. These results suggest that there may be two hormonal pathways involved with relaying sensory cues to the egg-laying circuitry, one involving
flp-1 and the other involving the Daf-c genes. We are currently investigating connections between the
flp-1 and daf pathways by constructing double mutants, and the results will be presented.