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Citation
Lloyd, T.E., Machamer, J., O'Hara, K., Kim, J.H., Collins, S.E., Wong, M.Y., Sahin, B., Imlach, W., Yang, Y., Levitan, E.S., McCabe, B.D., Kolodkin, A.L. (2012). The p150(Glued) CAP-Gly Domain Regulates Initiation of Retrograde Transport at Synaptic Termini.  Neuron 74(2): 344--360.
FlyBase ID
FBrf0218160
Publication Type
Research paper
Abstract

p150(Glued) is the major subunit of dynactin, a complex that functions with dynein in minus-end-directed microtubule transport. Mutations within the p150(Glued) CAP-Gly microtubule-binding domain cause neurodegenerative diseases through an unclear mechanism. A p150(Glued) motor neuron degenerative disease-associated mutation introduced into the Drosophila Glued locus generates a partial loss-of-function allele (Gl(G38S)) with impaired neurotransmitter release and adult-onset locomotor dysfunction. Disruption of the p150(Glued) CAP-Gly domain in neurons causes a specific disruption of vesicle trafficking at terminal boutons (TBs), the distal-most ends of synapses. Gl(G38S) larvae accumulate endosomes along with dynein and kinesin motor proteins within swollen TBs, and genetic analyses show that kinesin and p150(Glued) function cooperatively at TBs to coordinate transport. Therefore, the p150(Glued) CAP-Gly domain regulates dynein-mediated retrograde transport at synaptic termini, and this function of dynactin is disrupted by a mutation that causes motor neuron disease.

PubMed ID
PubMed Central ID
PMC3353876 (PMC) (EuropePMC)
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Neuron
    Title
    Neuron
    Publication Year
    1988-
    ISBN/ISSN
    0896-6273
    Data From Reference
    Alleles (33)
    Genes (23)
    Human Disease Models (2)
    Physical Interactions (5)
    Cell Lines (1)
    Natural transposons (2)
    Insertions (3)
    Experimental Tools (5)
    Transgenic Constructs (25)