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RAB-10 Regulates Glutamate Receptor Recycling in a Cholesterol-dependent Endocytosis Pathway

Glodowski, Doreen R., Chen, Carlos Chih-Hsiung, Schaefer, Henry, Grant, Barth D., Rongo, Christopher·2007·Molecular Biology of the Cell
DOI 10.1091/mbc.e07-05-0486
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Abstract

Regulated endocytosis of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-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 have not been fully characterized. Here, we examine the trafficking of the AMPAR subunit GLR-1 in Caenorhabditis 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 postsynaptic density 95/disc-large/zona occludens-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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  • The study extended the known Retromer regulators to include DENND4A and DENND4C, TBC1D13, and a TBC1D1/TBC1D4 heterodimer, establishing mechanistic links between Retromer and the switching of RAB10 and RAB35.

    “We have now extended these regulators to include DENND4A and DENND4C, TBC1D13, and a TBC1D1/TBC1D4 heterodimer, and in so doing, established mechanistic links between Retromer and the switching of RAB10 and RAB35; two RAB GTPases previously linked to the regulation of endosomal cargo recycling85,88–90,92,96,101,121,122.”

    From Mapping of endosomal proximity proteomes reveals Retromer as a hub for RAB GTPase regulation (2025) · cites this paper as [121]

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Metadata

Authors
Glodowski, D. R., Chen, C. C.-H., Schaefer, H., Grant, B. D., & Rongo, C.
Affiliations
  • *The Waksman Institute,
  • Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854
Venue
Molecular Biology of the Cell
Publisher
American Society for Cell Biology (ASCB)
Published
2007-11
Volume
18
Issue
11
Pages
4387-4396
ISSN
  • 1059-1524
  • 1939-4586
DOI
10.1091/mbc.e07-05-0486
Cited by
86
References
2
Language
en

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