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. Author manuscript; available in PMC: 2009 Oct 1.
Published in final edited form as: Nat Neurosci. 2009 Mar 15;12(4):387–389. doi: 10.1038/nn.2290

Fig. 1. Neuronal Wnd promotes axon degeneration in Drosophila.

Fig. 1

(a)GFP expressed in a subpopulation of ORNs using Or47b-Gal4 to visualize ORN axons. Before severing, the commissure shown in the boxed region is present in all genotypes. Higher power images of the commissural region taken twenty-four hours after axotomy show that (b) no axons remained in the commissure of most wildtype flies (14 of 46 flies had a commissure) and (c) axons are significantly preserved in the commissure of most wnd mutant flies (33 of 49 flies had a commissure). This reflects a delay of degeneration as remaining commissures were thinner than non-axotomized commissures, and wnd mutant flies reached wildtype levels of degeneration after forty-eight hours (data not shown). (d) When Wnd was exclusively expressed in the GFP expressing subpopulation of ORNs of otherwise wnd mutant flies, no axons were detected in the commissure of most flies (3 out of 20 flies had a commissure). Thus, Wnd promotes degeneration cell-autonomously. (e) Fraction of flies of each genotype with and without an ORN commissure. (Axons were significantly preserved in genotype c compared to both genotype b and genotype d, p < 0.005, and axons in genotype d were not preserved compared to genotype b, p > 0.25., X 2, two degrees of freedom). Scale bar = (a) 25 μm and (bd) 10 μm.