This research interestingly showed that the events that cause axon destruction do in fact morphologically resemble Wallerian degeneration in mammals: Severed axons remain intact for a defined latent phase of 6–8 h, then exhibit beading and cytoskeletal breakdown, and finally undergo complete fragmentation.
Similar to this, adult Drosophila brain primary cultures' PDF+ CNS axons that were cut showed degeneration within a day (Ayaz et al. 2008).
But looking at how WldS modifies disease models can provide some hints. There are two other theories for how damage causes Wallerian degeneration: either a prod generation signal produced at the location of the lesion (for example, calcium influx via the cut end) or the absence of a prosurvival signal coming from the cell body.
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