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Resources » Paper

Glodowski DR et al. (2007) Mol Biol Cell "RAB-10 regulates glutamate receptor recycling in a cholesterol-dependent endocytosis pathway."

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  • Comments on Glodowski DR et al. (2007) Mol Biol Cell "RAB-10 regulates glutamate receptor recycling in a cholesterol-dependent endocytosis pathway." (0)

  • Overview

    PMID:
    17761527
    DOI:
    10.1091/mbc.E07-05-0486
    Status:
    Publication type:
    Journal_article
    WormBase ID:
    WBPaper00030925

    Glodowski DR, Chen CC, Schaefer H, Grant BD, & Rongo C (2007). RAB-10 regulates glutamate receptor recycling in a cholesterol-dependent endocytosis pathway. Mol Biol Cell, 18, 4387-96. doi:10.1091/mbc.E07-05-0486

    Monitoring Editor: Tom U. Martin Regulated endocytosis of AMPA-type glutamate receptors (AMPARs) is critical for synaptic plasticity. However, the specific combination of clathrin-dependent and independent mechanisms that mediate AMPAR trafficking in vivo has not been fully characterized. Here we examine the trafficking of the AMPAR subunit GLR-1 in C. elegans. GLR-1 is localized on synaptic membranes, where it regulates reversals of locomotion in a simple behavioral circuit. Animals lacking RAB-10, a small GTPase required for endocytic recycling of intestinal cargo, are similar in phenotype to animals lacking LIN-10, a PDZ-domain containing protein: GLR-1 accumulates in large accretions and animals display a decreased frequency of reversals. Mutations in unc-11 (AP180) or itsn-1 (Intersectin 1), which reduce clathrin-dependent endocytosis, suppress the lin-10 but not rab-10 mutant phenotype, suggesting that LIN-10 functions after clathrin-mediated endocytosis. By contrast, cholesterol depletion, which impairs lipid raft formation and clathrin-independent endocytosis, suppresses the rab-10 but not the lin-10 phenotype, suggesting that RAB-10 functions after clathrin-independent endocytosis. Animals lacking both genes display additive GLR-1 trafficking defects. We propose that RAB-10 and LIN-10 recycle AMPARs from intracellular endosomal compartments to synapses along distinct pathways, each with distinct sensitivities to cholesterol and the clathrin-mediated endocytosis machinery.


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