We conclude that Ror promotes dendrite regeneration as part of a Wnt signaling pathway that regulates dendritic microtubule nucleation.Ĭitation: Nye DMR, Albertson RM, Weiner AT, Hertzler JI, Shorey M, Goberdhan DCI, et al. In addition, dendrite regeneration was sensitive to partial reduction of γTubulin. Consistent with this hypothesis, localization of the core nucleation protein γTubulin was reduced in Ror RNAi neurons, and this effect was strongest during dendrite regeneration. We therefore hypothesized that Ror may act by regulating microtubule nucleation at baseline and during dendrite regeneration. We recently found that Wnt signaling proteins, including dsh and Axin, localize microtubule nucleation machinery in dendrites. Moreover, Ror was required to position dsh and Axin in dendrites. We found that knockdown of fz, dishevelled (dsh), Axin, and gilgamesh (gish) also reduced dendrite regeneration. Ror can act as a Wnt coreceptor with frizzleds (fzs) in other contexts, so we tested the involvement of Wnt signaling proteins in dendrite regeneration. Ror was not required for axon regeneration or normal dendrite development, suggesting a specific role in dendrite regeneration. We confirmed that Ror was required for regeneration in two different neuron types using RNA interference (RNAi) and mutants. Using a Drosophila model of dendrite regeneration, we performed a candidate screen of receptor tyrosine kinases (RTKs) and found a requirement for RTK-like orphan receptor (Ror). While many regulators of axon regeneration have been identified, very little is known about mechanisms that allow dendrites to regenerate after injury.
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