Figure 7. Constitutively active AMPK rescues Rheb-mediated axon guidance and phototaxis deficits, but not NMJ overgrowth or amplified EJP responses.

(A–C) Expression of a constitutively activated AMPK transgene together with Rheb⁺ greatly decreased the severity of the axon misrouting defects (arrows) normally seen in Rheb–overexpressing animals. (D) Co-expression of both AMPK^TD and Rheb⁺ in neurons also rescued the phototaxis deficits normally present in Rheb-expressing animals. When we expressed AMPK^TD on its own, we did not see any change in phototaxis performance compared to controls or any measurable axon misrouting (data not shown). (E–H) At the larval NMJ, co-expression of a constitutively-activated AMPK in Rheb-overexpressing neurons did not rescue Rheb-mediated synaptic overgrowth, and in fact, caused an even greater increase in synapse size, despite the fact that AMPK^TD had no effect on synapse growth when expressed on its own. (I) Similarly, co-expression of AMPK^TD in Rheb-overexpressing neurons failed to rescue the elevated EJP amplitudes and, in fact, further exacerbated this defect. AMPK ^TD had no effect on synaptic response when expressed alone. Asterisks denote a two-tailed Student's t-test statistic of p<0.05. Scale bars are 50 microns.