OA and TA can act both inside and outside of the nervous system,
functioning as either a neurotransmitter or a neurohormone in insects
Cole 2005. Thus, we explored whether the sugar response
phenotype of tßh mutants was a result of alterations in
neurons inside or outside of the brain or in non-neuronal cells. To this end, we expressed tßh in tßhnM18
mutant males using different GAL4-lines. We found a significant
increase in sugar response compared to the respective mutant control
when we used the ubiquitous Actin-promoter to drive Gal4 in all cells, the pan-neuronal
nSyb-promoter, or the non-neuronal Tdc1-GAL4 driver (Fig. 6). In
contrast, tßh expression in subsets of OA/TA-neurons, using either Tdc2- or NP7088-GAL4 did not
significantly affect the mutants’ response (Fig. 6), in contrast to a
previous report (NP7088-Gal4, Scheiner 2014). These last two results also show that the UAS construct alone is not sufficient to bring a rescue. These results
indicate that tßh expression induced in neurons in the
central nervous system or in non-neuronal cells, respectively, is sufficient
to enhance the sugar responsiveness of tßhnM18 mutant flies.