Effects of losses of <i>aak-1</i> and <i>tph-1</i> on <i>aak-2</i> mutant phenotypes.

<p><b>A-C.</b> Phenotypes of <i>aak-2</i> loss of function are not dependent on <i>aak-1</i>. Feeding (A), movement (B), and hypodermal BODIPY staining levels (C) of <i>aak-1; aak-2</i> double mutants are not significantly different than those of <i>aak-2</i> mutants. For feeding, movement and BODIPY measurements, n = 10, *p<0.05, Student's t-test. Error bars represent +/−SEM. <b>D-F.</b> Loss of <i>aak-2</i> elicits feeding (D), movement (E), and fat phenotypes (<b>F</b>) even in serotonin deficient <i>tph-1</i> mutants. The feeding rate of <i>tph-1; aak-2</i> mutants was significantly different than both <i>tph-1</i> and <i>aak-2</i> single mutants (D). <i>tph-1; aak-2</i> double mutants moved significantly more slowly than <i>tph-1</i> or WT but statistically indistinguishable than <i>aak-2</i> mutants off of food (E) For BODIPY staining in the hypodermal head region, loss <i>aak-2</i> further reduced the already low hypodermal head staining of <i>tph-1</i> 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 <i>tph-1</i> 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 <i>tph-1</i> with <i>tph-1; aak-2.</i></p>