Questions, Feedback & Help
Send us an email and we'll get back to you ASAP. Or you can read our Frequently Asked Questions.
  • page settings
  • hide sidebar
  • show empty fields
  • layout
  • (too narrow)
  • open all
  • close all
Resources » Paper

Garafalo, Steven D. et al. (2013) International Worm Meeting "The AP2 clathrin adaptor subunit APM-2 regulates the abundance of GLR-1 glutamate receptors in the ventral nerve cord of C. elegans."

  • History

  • Referenced

  • Tree Display

  • My Favorites

  • My Library

  • Comments on Garafalo, Steven D. et al. (2013) International Worm Meeting "The AP2 clathrin adaptor subunit APM-2 regulates the abundance of GLR-1 glutamate receptors in the ventral nerve cord of C. elegans." (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00043393

    Garafalo, Steven D., Dahlberg, Caroline L., Malkin, Emily, & Juo, Peter (2013). The AP2 clathrin adaptor subunit APM-2 regulates the abundance of GLR-1 glutamate receptors in the ventral nerve cord of C. elegans presented in International Worm Meeting. Unpublished information; cite only with author permission.

    Glutamate receptors (GluRs) mediate the majority of excitatory neurotransmission in the central nervous system. Regulation of the postsynaptic abundance of GluRs controls the strength of synaptic transmission which plays a critical role in learning and memory. We are interested in identifying genes and mechanisms involved in trafficking GLR-1 GluRs to synapses in the ventral nerve cord (VNC). GLR-1 is an AMPA-type GluR which is expressed in interneurons and localized to synapses in the VNC. Here, we show that APM-2 (also known as DPY-23), the m2 subunit of the clathrin adaptor AP2, regulates the abundance of GLR-1 in the VNC. AP2 is well known as a regulator of clathrin-mediated endocytosis at the plasma membrane. Surprisingly, we found that apm-2(gm17) and apm-2(e840) loss-of-function mutants have reduced levels of GLR-1 in the VNC. This effect can be rescued by expression of wild type apm-2 cDNA in the glr-1-expressing interneurons. In addition, expression of apm-2 under a heat-shock inducible promoter at the L4 stage can rescue the GLR-1 defect observed in apm-2 mutants, suggesting that APM-2 can function in the mature nervous system to regulate GLR-1. In contrast, mutation of another clathrin adaptin UNC-11/AP180, which regulates endocytosis of GLR-1 at synapses, results in accumulation of GLR-1 in the VNC. Interestingly, apm-2;unc-11 double mutants exhibit reduced levels of GLR-1 at synapses suggesting that apm-2 functions prior to GLR-1 endocytosis in the VNC. We hypothesize that APM-2 regulates anterograde trafficking of GLR-1 from the cell body to synapses. Consistent with this idea, GLR-1 accumulates in cell bodies of apm-2 mutants and genetic double mutant analysis indicates that apm-2 functions in the same pathway as the kinesin klp-4, which is involved in anterograde transport of GLR-1. Our data reveal a novel function for APM-2 in regulating the levels of GLR-1 in the VNC and suggest that APM-2, and possibly the AP2 complex, regulate anterograde trafficking of GluRs. Several possible models of how APM-2 regulates GLR-1 trafficking will be discussed.

    Affiliation:
    - Molecular Physiology & Pharmacology, Tufts University School of Medicine, Boston, MA


    Tip: Seeing your name marked red? Please help us identify you.