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. 2015 Mar 30;208(7):931–947. doi: 10.1083/jcb.201404066

Figure 8.

Figure 8.

Rab8 mutants reveal a role for the JNKKK TAK1 in synaptic overgrowth at the NMJ. (A and B) Loss of TAK1 function generated by Inhibition of TAK1 through panneuronal (n-Syb–Gal4) expression of a dominant-negative form of TAK1, knockdown by TAK1-RNAi, or use of a TAK1 loss-of-function allele completely alleviated synaptic overgrowth in a Rab8 mutant background. Correspondingly panneuronal expression of UAS-TAK1 promotes synaptic overgrowth, characterized by a significant increase in synaptic bouton number. Reduction of HRS function, using a heterozygous HRS loss-of-function allele HRSD28/+, in combination with Rab81/+ elicited a significant increase in synaptic bouton number. HRSD28/+ or Rab81/+ alone did not affect bouton number. Bar, 10 µm. ANOVA: F (d.f. 11) = 24.2733; P < 0.001 with post-hoc Dunnett’s comparison to wild-type control: ***, P < 0.001. Student’s t test comparison between genotypes: ###, P < 0.001; #, P < 0.05. Numbers above bars = n. Error bars show SEM.