SNX9 family mediates βarrestin-independent GPCR endocytosis
Agonist-stimulated GPCR endocytosis typically occurs via the multi-faceted adaptor proteins known as βarrestins. However, endocytosis of several GPCRs occurs independently of β-arrestins, suggesting an additional mode of GPCR endocytosis, but the mechanisms remain unknown. Here we provide evidence that sorting nexin 9 (SNX9), a previously described endocytic remodeling protein, functions as a novel cargo adaptor that promotes agonist-stimulated GPCR endocytosis. We show that SNX9 and SNX18, but not β-arrestins, are necessary for endocytosis of the chemokine receptor CXCR4. SNX9 is recruited to CXCR4 at the plasma membrane and interacts directly with the carboxyl-terminal tail of the receptor in a phosphorylation-dependent manner. We also provide evidence that some receptors do not require SNX9 and SNX18 nor β-arrestins for endocytosis, suggesting additional modes for GPCR endocytosis. These results provide novel insights into the mechanisms regulating GPCR trafficking and broaden our overall understanding of GPCR regulation.
Authors
- Joseph M. Crecelius (ORCID: https://orcid.org/0000-0003-2370-9154)
- Adriano Marchese
- Sara Benzow
- Valeria L. Robleto (ORCID: https://orcid.org/0000-0002-1798-753X)
- Ya Zhuo (ORCID: https://orcid.org/0000-0002-3068-3792)
Institutions
- Medical College of Wisconsin (US)
Publication Details
- Journal
- Communications Biology
- Published
- 2024-11-07
- DOI
- https://doi.org/10.1038/s42003-024-07157-7
- Citations
- 6
- Primary Topic
- Receptor Mechanisms and Signaling
- Type
- article
- Field-Weighted Citation Impact
- 1.40
Funders
- Institute for Research in Biomedicine
- National Institutes of Health