Effects of mutations that downregulate the Tor pathway on photoreceptor axon guidance, and genetic epistasis with <i>Tsc1</i>.

<p>Optic lobes from third instar larvae (A–C) and 40h pupae (D–F) stained with MAb24B10. (A) Larvae heteroallelic for a hypomorphic combination of <i>Rheb</i> alleles show abnormal photoreceptor patterning and contain thick axon bundles that extend into the medulla (arrowhead). (D) At the 40 h pupal stage, <i>Rheb</i> mutants display axons that bypass their normal targets in the R7/R8 termination zones (arrowhead). (B) Larvae homozygous for a hypomorphic <i>Tor</i> allele show fairly normal photoreceptor patterning, but at the pupal stage (E) misrouted axons can be seen in the medulla (arrowheads). (C) <i>S6k</i> null homozygous larvae show thick axon bundles projecting past the lamina (arrowhead), while <i>S6k</i> pupae (F) display misrouted axons that initially bypass the R7/R8 termination zone (arrowhead). (G, H) Animals doubly mutant for <i>Tor</i> and <i>Tsc1</i> do not show the severe photoreceptor defects seen when axons are mutant for <i>Tsc1</i> alone (compare to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0000375#pone-0000375-g005" target="_blank">Figure 5B, F, F′</a>), although mild defects similar to those in <i>Tor</i> mutants are still apparent (arrowhead). (I) <i>S6k-Tsc1</i> double homozygous mutants display a severe phenotype dissimilar to mutants for either <i>S6k</i> or <i>Tsc1</i> alone. The scale bar is 25 microns in panel A, 50 microns in panel D.