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    Spatially resolved phosphoproteomics reveals fibroblast growth factor receptor recycling-driven regulation of autophagy and survival

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    Authors
    Watson, J.
    Ferguson, H. R.
    Brady, Rosie M
    Ferguson, J.
    Fullwood, P.
    Mo, H.
    Bexley, K. H.
    Knight, D.
    Howell, G.
    Schwartz, J. M.
    Smith, M. P.
    Francavilla, C.
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    Affiliation
    Division of Evolution, Infection and Genomics, School of Biological Science, Faculty of Biology Medicine and Health (FBMH), The University of Manchester, M139PT, Manchester, UK
    Issue Date
    2022
    
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    Abstract
    Receptor Tyrosine Kinase (RTK) endocytosis-dependent signalling drives cell proliferation and motility during development and adult homeostasis, but is dysregulated in diseases, including cancer. The recruitment of RTK signalling partners during endocytosis, specifically during recycling to the plasma membrane, is still unknown. Focusing on Fibroblast Growth Factor Receptor 2b (FGFR2b) recycling, we reveal FGFR signalling partners proximal to recycling endosomes by developing a Spatially Resolved Phosphoproteomics (SRP) approach based on APEX2-driven biotinylation followed by phosphorylated peptides enrichment. Combining this with traditional phosphoproteomics, bioinformatics, and targeted assays, we uncover that FGFR2b stimulated by its recycling ligand FGF10 activates mTOR-dependent signalling and ULK1 at the recycling endosomes, leading to autophagy suppression and cell survival. This adds to the growing importance of RTK recycling in orchestrating cell fate and suggests a therapeutically targetable vulnerability in ligand-responsive cancer cells. Integrating SRP with other systems biology approaches provides a powerful tool to spatially resolve cellular signalling.
    Citation
    Watson J, Ferguson HR, Brady RM, Ferguson J, Fullwood P, Mo H, et al. Spatially resolved phosphoproteomics reveals fibroblast growth factor receptor recycling-driven regulation of autophagy and survival. Nature communications. 2022 Nov 3;13(1):6589. PubMed PMID: 36329028. Pubmed Central PMCID: PMC9633600. Epub 2022/11/05. eng.
    Journal
    Nature Communications
    URI
    http://hdl.handle.net/10541/625755
    DOI
    10.1038/s41467-022-34298-2
    PubMed ID
    36329028
    Additional Links
    https://dx.doi.org/10.1038/s41467-022-34298-2
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41467-022-34298-2
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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