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. Author manuscript; available in PMC: 2012 Feb 15.
Published in final edited form as: J Neurosci. 2012 Jan 11;32(2):610–615. doi: 10.1523/JNEUROSCI.3586-11.2012

Figure 4.

Figure 4

The protective effect of the conditioning lesion requires Wallenda. A, Staining for endogenous Futsch in the segmental nerves of axons treated with conditioning lesion, as outlined in Figure 3A. In wnd1/wnd2 mutants, endogenous Futsch was fragmented similarly to control, singly injured axons (Fig. 1C). B, The m12-Gal4 driver line was used to drive expression of wnd-RNAi (along with UAS-Dcr2) or Fos DN in the GFP-labeled axons. The mCD8::GFP labeled axons are shown alone in grayscale (right). All axons were treated with a conditioning lesion with a Tc of 24 h, and the middle stump is shown 16 h after the second injury. Scale bars, 25 μm. C, Quantification of the axon degeneration index indicates that expression of wnd RNAi or Fos DN nearly completely abolishes the protective effect of the conditioning lesion. D, Model for the role of Wallenda, which becomes activated in axons by injury and mediates a signaling cascade that requires time and the Fos transcription factor. The downstream cellular changes that alter resiliency to degeneration remain to be determined.