作者: Derek M. R. Nye , Richard M. Albertson , Alexis T. Weiner , J. Ian Hertzler , Matthew Shorey
DOI: 10.1371/JOURNAL.PBIO.3000657
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摘要: While many regulators of axon regeneration have been identified, very little is known about mechanisms that allow dendrites to regenerate after injury. Using a Drosophila model dendrite regeneration, we performed candidate screen receptor tyrosine kinases (RTKs) and found requirement for RTK-like orphan (Ror). We confirmed Ror was required in two different neuron types using RNA interference (RNAi) mutants. not or normal development, suggesting specific role regeneration. can act as Wnt coreceptor with frizzleds (fzs) other contexts, so tested the involvement signaling proteins knockdown fz, dishevelled (dsh), Axin, gilgamesh (gish) also reduced Moreover, position dsh Axin dendrites. recently proteins, including localize microtubule nucleation machinery therefore hypothesized may by regulating at baseline during Consistent this hypothesis, localization core protein γTubulin RNAi neurons, effect strongest In addition, sensitive partial reduction γTubulin. conclude promotes part pathway regulates dendritic nucleation.