The expression of atl^HMS01627 under the control of Scer\GAL4²²¹ in larval ddaE neurons leads to defects in axon regeneration, shown by a significant decrease in axon length and by a lower recruitment of endoplasmic reticulum to the axon tip (marked by fluorescent Rtnl1), but not in dendrite regeneration, shown by a similar dendrite number, at 96h after laser-induced severance, as compared to controls. These neuron show an apparently normal early response to injury, since the pool of growing microtubules (identified as fluorescent EB1 comets) shows the expected increase in number and the expected reversal of polarity at 24h after laser-induced severance, as compared to controls. Uninjured atl^HMS01627-expressing neurons shown no obvious endoplasmic reticulum defects, as compared to controls.