Effects of losses of aak-1 and tph-1 on aak-2 mutant phenotypes.

A-C. Phenotypes of aak-2 loss of function are not dependent on aak-1. Feeding (A), movement (B), and hypodermal BODIPY staining levels (C) of aak-1; aak-2 double mutants are not significantly different than those of aak-2 mutants. For feeding, movement and BODIPY measurements, n = 10, *p<0.05, Student's t-test. Error bars represent +/−SEM. D-F. Loss of aak-2 elicits feeding (D), movement (E), and fat phenotypes (F) even in serotonin deficient tph-1 mutants. The feeding rate of tph-1; aak-2 mutants was significantly different than both tph-1 and aak-2 single mutants (D). tph-1; aak-2 double mutants moved significantly more slowly than tph-1 or WT but statistically indistinguishable than aak-2 mutants off of food (E) For BODIPY staining in the hypodermal head region, loss aak-2 further reduced the already low hypodermal head staining of tph-1 mutants (F). For feeding, movement and BODIPY measurements, n = 10, *p<0.05, Student's t-test. Error bars represent +/−SEM. Please note that the BODIPY quantitations are of the head hypodermal region only. While tph-1 mutants have been reported to have elevated intestinal fat levels, their head hypodermal region actually has less staining relative to WT animals. To be consistent with our various other BODIPY measurements, we have concentrated on the same head hypodermal region when comparing tph-1 with tph-1; aak-2.