NECAP2 controls clathrin coat recruitment to early endosomes for fast endocytic recycling
| Autor: | Lauren T. Antonow, Brigitte Ritter, Michel Dias Santos, John P. Chamberland |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Endosome Endocytic cycle Endocytic recycling Transferrin receptor Endosomes Biology Endocytosis Clathrin coat Clathrin 03 medical and health sciences Humans Cell Membrane Transferrin Membrane Proteins Clathrin-Coated Vesicles Cell Biology Fast endocytic recycling Cell biology Adaptor Protein Complex Subunits ErbB Receptors Adaptor Proteins Vesicular Transport Protein Transport 030104 developmental biology biology.protein HeLa Cells Protein Binding |
| Zdroj: | Journal of cell science. 129(13) |
| ISSN: | 1477-9137 |
| Popis: | Endocytic recycling returns receptors to the plasma membrane following internalization and is essential to maintain receptor levels on the cell surface, resensitize cells to extracellular ligands and for continued nutrient uptake. Yet, the protein machineries and mechanisms driving endocytic recycling remain ill-defined. Here, we establish that NECAP2 regulates the endocytic recycling of EGFR and transferrin receptor. Our analysis of the recycling dynamics revealed that NECAP2 functions in the fast recycling pathway that directly returns cargo from early endosomes to the cell surface. In contrast, NECAP2 does not regulate the clathrin-mediated endocytosis of these cargo, the degradation of EGFR, or the recycling of transferrin along the slow, Rab11-dependent recycling pathway. We show that protein knock-down of NECAP2 leads to enlarged early endosomes and causes the loss of the clathrin adapter AP-1 from the organelle. Through structure-function analysis, we define the protein binding interfaces in NECAP2 that are critical for AP-1 recruitment to early endosomes. Together, our data identify NECAP2 as a pathway-specific regulator of clathrin coat formation on early endosomes for fast endocytic recycling. |
| Databáze: | OpenAIRE |
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