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Citation
Lin, W.Y., Williams, C., Yan, C., Koledachkina, T., Luedke, K., Dalton, J., Bloomsburg, S., Morrison, N., Duncan, K.E., Kim, C.C., Parrish, J.Z. (2015). The SLC36 transporter Pathetic is required for extreme dendrite growth in Drosophila sensory neurons.  Genes Dev. 29(11): 1120--1135.
FlyBase ID
FBrf0228679
Publication Type
Research paper
Abstract

Dendrites exhibit enormous diversity in form and can differ in size by several orders of magnitude even in a single animal. However, whether neurons with large dendrite arbors have specialized mechanisms to support their growth demands is unknown. To address this question, we conducted a genetic screen for mutations that differentially affected growth in neurons with different-sized dendrite arbors. From this screen, we identified a mutant that selectively affects dendrite growth in neurons with large dendrite arbors without affecting dendrite growth in neurons with small dendrite arbors or the animal overall. This mutant disrupts a putative amino acid transporter, Pathetic (Path), that localizes to the cell surface and endolysosomal compartments in neurons. Although Path is broadly expressed in neurons and nonneuronal cells, mutation of path impinges on nutrient responses and protein homeostasis specifically in neurons with large dendrite arbors but not in other cells. Altogether, our results demonstrate that specialized molecular mechanisms exist to support growth demands in neurons with large dendrite arbors and define Path as a founding member of this growth program.

PubMed ID
PubMed Central ID
PMC4470281 (PMC) (EuropePMC)
Related Publication(s)
Personal communication to FlyBase

Location data for the path[dg50] deletion.
Lin and Parrish, 2016.1.15, Location data for the path[dg50] deletion. [FBrf0230718]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Genes Dev.
    Title
    Genes & Development
    Publication Year
    1987-
    ISBN/ISSN
    0890-9369
    Data From Reference
    Aberrations (1)
    Alleles (49)
    Genes (30)
    Natural transposons (2)
    Insertions (17)
    Experimental Tools (6)
    Transgenic Constructs (30)
    Transcripts (3)