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Citation
Tian, X., Li, J., Valakh, V., Diantonio, A., Wu, C. (2011). Drosophila Rae1 controls the abundance of the ubiquitin ligase Highwire in post-mitotic neurons.  Nat. Neurosci. 14(10): 1267--1275.
FlyBase ID
FBrf0216253
Publication Type
Research paper
Abstract

The evolutionarily conserved Highwire (Hiw)/Drosophila Fsn E3 ubiquitin ligase complex is required for normal synaptic morphology during development and axonal regeneration after injury. However, little is known about the molecular mechanisms that regulate the Hiw E3 ligase complex. Using tandem affinity purification techniques, we identified Drosophila Rae1 as a previously unknown component of the Hiw/Fsn complex. Loss of Rae1 function in neurons results in morphological defects at the neuromuscular junction that are similar to those seen in hiw mutants. We found that Rae1 physically and genetically interacts with Hiw and restrains synaptic terminal growth by regulating the MAP kinase kinase kinase Wallenda. Moreover, we found that the Rae1 is both necessary and sufficient to promote Hiw protein abundance, and it does so by binding to Hiw and protecting Hiw from autophagy-mediated degradation. These results describe a previously unknown mechanism that selectively controls Hiw protein abundance during synaptic development.

PubMed ID
PubMed Central ID
PMC3183334 (PMC) (EuropePMC)
Related Publication(s)
Note

Maintaining a Highwire act.
Spencer, 2011, Nat. Neurosci. 14(10): 1226 [FBrf0216599]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Nat. Neurosci.
    Title
    Nature Neuroscience
    Publication Year
    1998-
    ISBN/ISSN
    1097-6256
    Data From Reference