Autophagy captures the retromer-TBC1D5 complex to inhibit receptor recycling

Date

2024

Authors

Carosi, J.M.
Hein, L.K.
Sandow, J.J.
Dang, L.V.P.
Hattersley, K.
Denton, D.
Kumar, S.
Sargeant, T.J.

Editors

Advisors

Journal Title

Journal ISSN

Volume Title

Type:

Journal article

Citation

Autophagy, 2024; 20(4):863-882

Statement of Responsibility

Julian M. Carosi, Leanne K. Hein, Jarrod J. Sandow, Linh V. P. Dang, Kathryn Hattersley, Donna Denton, Sharad Kumar and Timothy J. Sargeant

Conference Name

Abstract

Retromer prevents the destruction of numerous receptors by recycling them from endosomes to the trans-Golgi network or plasma membrane. This enables retromer to fine-tune the activity of many signaling pathways in parallel. However, the mechanism(s) by which retromer function adapts to environmental fluctuations such as nutrient withdrawal and how this affects the fate of its cargoes remains incompletely understood. Here, we reveal that macroautophagy/autophagy inhibition by MTORC1 controls the abundance of retromer+ endosomes under nutrient-replete conditions. Autophagy activation by chemical inhibition of MTOR or nutrient withdrawal does not affect retromer assembly or its interaction with the RAB7 GAP protein TBC1D5, but rather targets these endosomes for bulk destruction following their capture by phagophores. This process appears to be distinct from amphisome formation. TBC1D5 and its ability to bind to retromer, but not its C-terminal LC3-interacting region (LIR) or nutrient-regulated dephosphorylation, is critical for retromer to be captured by autophagosomes following MTOR inhibition. Consequently, endosomal recycling of its cargoes to the plasma membrane and trans-Golgi network is impaired, leading to their lysosomal turnover. These findings demonstrate a mechanistic link connecting nutrient abundance to receptor homeostasis.

School/Discipline

Dissertation Note

Provenance

Description

Published online: 17 Nov 2023 Data source: Supplemental data, https://doi.org/10.1080/15548627.2023.2281126

Access Status

Rights

© 2024 Informa UK Limited, trading as Taylor & Francis Group

License

Call number

Persistent link to this record