Publications by authors named "Dylan Y Seebold"
Axon regeneration in response to injury has been documented in many animals over several hundred years. In contrast, how neurons respond to dendrite injury has been examined only in the last decade. So far, dendrite regeneration after injury has been documented in invertebrate model systems, but has not been assayed in a vertebrate.
View Article and Find Full Text PDFDendrite microtubules are polarized with minus-end-out orientation in Drosophila neurons. Nucleation sites concentrate at dendrite branch points, but how they localize is not known. Using Drosophila, we found that canonical Wnt signaling proteins regulate localization of the core nucleation protein γTubulin (γTub).
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- Microtubule minus ends, typically considered stable, were found to exhibit persistent growth in neurons of zebrafish and other species, lasting over 10 minutes.
- The growth of these minus ends relies on a protein called Patronin, whose reduction disrupts the polarity of dendrites by decreasing minus-end-out microtubules.
- Increased Patronin levels result in dendrites predominantly exhibiting minus-end-out microtubules, highlighting its role in maintaining microtubule orientation necessary for dendritic growth and regeneration.
In neurons, uniform minus-end-out polarity in dendrites is maintained in part by kinesin-2-mediated steering of growing microtubules at branch points. Apc links the kinesin motor to growing microtubule plus ends and Apc2 recruits Apc to branch points where it functions. Because Apc2 acts to concentrate other steering proteins to branch points, we wished to understand how Apc2 is targeted.
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