Fig. 2.

JNK axon degeneration is not caused by aberrant axonal pruning or myosin-based retraction or affected by apoptotic inhibitors. (A–C) Overexpressing a dominant-negative (DN) form of EcR-B1 (A) or the ubiquitin protease UBP-2 (B) in bsk^147e MB neuroblast clones fails to suppress the JNK axon degeneration phenotype in either γ- or β-neurons (blue and yellow arrows, respectively). MB neuroblast clones were analyzed at 14 days post-eclosion. (C) Dominant-negative Zipper (DN Zip) expression also fails to rescue the bsk degeneration phenotype. (D–F) Overexpression of anti-apoptotic regulators including Diap1 (D), a dominant-negative (DN) form of Dronc (E) or Buffy (F) does not suppress JNK degeneration phenotype. Green, CD8-GFP (neurons); magenta, FasII (axons). Scale bar: 20 µm. (G) Quantification of β-axon degeneration in JNK-null genotypes in the presence of the indicated transgenes. n indicates the number of MB neuroblast clones analyzed. No significant differences were found between age-matched bsk^147e mutant and bsk^147e UAS coexpression genotypes (P>0.05; using Fisher's exact test).