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• W3202373309 abstract "Removal of damaged organelles via the process of selective autophagy constitutes a major form of cellular quality control. Damaged organelles are recognized by a dedicated surveillance machinery, leading to the assembly of an autophagosome around the damaged organelle, prior to fusion with the degradative lysosomal compartment. Lysosomes themselves are also prone to damage and are degraded through the process of lysophagy. While early steps involve recognition of ruptured lysosomal membranes by glycan-binding galectins and ubiquitylation of transmembrane lysosomal proteins, many steps in the process, and their interrelationships, remain poorly understood, including the role and identity of cargo receptors required for completion of lysophagy. Here, we employ quantitative organelle capture and proximity biotinylation proteomics of autophagy adaptors, cargo receptors, and galectins in response to acute lysosomal damage, thereby revealing the landscape of lysosome-associated proteome remodeling during lysophagy. Among the proteins dynamically recruited to damaged lysosomes were ubiquitin-binding autophagic cargo receptors. Using newly developed lysophagic flux reporters including Lyso-Keima, we demonstrate that TAX1BP1, together with its associated kinase TBK1, are both necessary and sufficient to promote lysophagic flux in both HeLa cells and induced neurons (iNeurons). While the related receptor Optineurin (OPTN) can drive damage-dependent lysophagy when overexpressed, cells lacking either OPTN or CALCOCO2 still maintain significant lysophagic flux in HeLa cells. Mechanistically, TAX1BP1-driven lysophagy requires its N-terminal SKICH domain, which binds both TBK1 and the autophagy regulatory factor RB1CC1, and requires upstream ubiquitylation events for efficient recruitment and lysophagic flux. These results identify TAX1BP1 as a central component in the lysophagy pathway and provide a proteomic resource for future studies of the lysophagy process." @default.
• W3202373309 created "2021-10-11" @default.
• W3202373309 creator A5019693269 @default.
• W3202373309 creator A5026734370 @default.
• W3202373309 creator A5035448367 @default.
• W3202373309 creator A5053069378 @default.
• W3202373309 creator A5085158845 @default.
• W3202373309 date "2021-09-29" @default.
• W3202373309 modified "2023-10-17" @default.
• W3202373309 title "Quantitative proteomics reveals the selectivity of ubiquitin-binding autophagy receptors in the turnover of damaged lysosomes by lysophagy" @default.
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• W3202373309 doi "https://doi.org/10.7554/elife.72328" @default.
• W3202373309 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8523161" @default.
• W3202373309 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34585663" @default.
• W3202373309 hasPublicationYear "2021" @default.

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