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Li, J., Zhang, Y.V., Asghari Adib, E., Stanchev, D.T., Xiong, X., Klinedinst, S., Soppina, P., Jahn, T.R., Hume, R.I., Rasse, T.M., Collins, C.A. (2017). Restraint of presynaptic protein levels by Wnd/DLK signaling mediates synaptic defects associated with the kinesin-3 motor Unc-104.  eLife 6(): e24271.
FlyBase ID
FBrf0236772
Publication Type
Research paper
Abstract

The kinesin-3 family member Unc-104/KIF1A is required for axonal transport of many presynaptic components to synapses, and mutation of this gene results in synaptic dysfunction in mice, flies and worms. Our studies at the Drosophila neuromuscular junction indicate that many synaptic defects in unc-104-null mutants are mediated independently of Unc-104's transport function, via the Wallenda (Wnd)/DLK MAP kinase axonal damage signaling pathway. Wnd signaling becomes activated when Unc-104's function is disrupted, and leads to impairment of synaptic structure and function by restraining the expression level of active zone (AZ) and synaptic vesicle (SV) components. This action concomitantly suppresses the buildup of synaptic proteins in neuronal cell bodies, hence may play an adaptive role to stresses that impair axonal transport. Wnd signaling also becomes activated when pre-synaptic proteins are over-expressed, suggesting the existence of a feedback circuit to match synaptic protein levels to the transport capacity of the axon.

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PubMed Central ID
PMC5605197 (PMC) (EuropePMC)
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    Language of Publication
    English
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    Parent Publication
    Publication Type
    Journal
    Abbreviation
    eLife
    Title
    eLife
    ISBN/ISSN
    2050-084X
    Data From Reference
    Aberrations (1)
    Alleles (42)
    Genes (17)
    Human Disease Models (1)
    Natural transposons (1)
    Insertions (11)
    Experimental Tools (2)
    Transgenic Constructs (19)