Genetic rescues of <i>AC3</i> knockdown and over-expression effects in M cells.

<p>(A) Rescuing the loss of function state. Flies were raised at 25°C and moved to 18°C as adults for 12–15 h before imaging to reduce levels of <i>AC3</i> over-expression. The effect of this schedule on the effects of <i>AC3</i> knockdown (TRiP:<i>AC3</i>RNAi) and <i>AC3</i> over-expression (UAS-<i>AC3</i>) is shown. The ability of over-expressing <i>AC78C</i> (TRiP:<i>AC3</i>/UAS<i>AC78C</i>) and <i>AC3</i> (TRiP:<i>AC3</i>RNAi/UAS<i>AC3</i>) to reverse the knockdown effect of <i>AC3</i> RNAi are also shown. (B) Rescuing the gain of function state. Two <i>PDF-R</i> over-expression genotypes were tested for their ability to affect <i>AC3</i> over-expression: a UAS construct (UAS<i>PDF-R</i>;UAS<i>AC3</i>) and a construct in which <i>PDF-R</i> is driven by its endogenous promotor (UAS<i>AC3</i>;<i>PDF-R</i>myc). For comparison the effects of co-misexpressing a heterologous neuropeptide receptor is also shown (UAS<i>DH31R</i>/UAS<i>AC3</i>). All genotypes include <i>Pdf</i>-gal4;<i>Epac1camps</i>. Error bars denote SEM. *** <i>p</i><0.001, * <i>p</i><.05 (compared with control).