γ-secretase facilitates retromer-mediated retrograde transport
Retromer mediates retrograde transport of protein cargoes from endosomes to the trans-Golgi network (TGN). γ-secretase is a protease that cleaves the transmembrane domain of its target proteins. Although retromer can form a stable complex with γ-secretase, the functional consequences of this interaction are not known. Here, we report that retromer-mediated retrograde protein trafficking in cultured human epithelial cells is impaired by the γ-secretase inhibitor XXI or by knockout of PS1 (also known as PSEN1), the catalytic subunit of γ-secretase. These treatments inhibited endosome-to-TGN trafficking of retromer-dependent retrograde cellular cargoes, divalent metal transporter 1 isoform II, cation-independent mannose-6-phosphate receptor and shiga toxin, whereas trafficking of retromer-independent cargoes, cholera toxin and a mutant CIMPR unable to bind retromer was not affected. Moreover, we found that γ-secretase associates with retromer cargoes even in the absence of retromer. XXI treatment and PS1 knockout did not inhibit the ability of retromer or γ-secretase to associate with cargo and did not affect the expression of retromer subunits or Rab7-GTP, which regulates retromer-cargo interaction. These results imply that the γ-secretase-retromer interaction facilitates retromer-mediated retrograde trafficking of cellular transmembrane proteins.
Authors
- Mac Crite (ORCID: https://orcid.org/0000-0001-8225-5143)
- Daniel DiMaio (ORCID: https://orcid.org/0000-0002-2060-5977)
- Kashif Mehmood (ORCID: https://orcid.org/0000-0001-6805-9306)
- Yuka Takeo (ORCID: https://orcid.org/0000-0002-2911-4322)
Institutions
- Yale Cancer Center (US)
- Yale University (US)
Publication Details
- Journal
- Journal of Cell Science
- Published
- 2025-01-27
- DOI
- https://doi.org/10.1242/jcs.263538
- Citations
- 1
- Primary Topic
- Cellular transport and secretion
- Type
- article
- Field-Weighted Citation Impact
- 1.15
Funders
- Yale University
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases