Left, soluble SARs such as SQSTM1/p62, NDP52, OPTN, TAX1BP1, and NBR1 are cytosolic proteins that are recruited to cargo on demand. Their recruitment is commonly driven by ubiquitin (Ub) marks on damaged or misfolded cargo, enabling rapid and flexible targeting of diverse substrates. Upon recruitment, these SARs concentrate autophagy initiation factors at the cargo site to initiate autophagosome biogenesis. Right, transmembrane SARs such as NIX, BNIP3, FAM134B, and CCPG1 are stably integrated within organelle membranes. To prevent unwanted autophagy activation, these SARs require additional layers of control. Selective autophagy can be triggered by transcriptional upregulation (e.g., hypoxia-driven induction of NIX/BNIP3), post-translational modifications such as ubiquitination, or SAR clustering. ER-phagy SARs further promote local membrane bending and scission to excise a portion of the organelle for autophagic removal. While some SARs are transcriptionally induced, others—such as FAM134B—are constitutively present and rely primarily on clustering and post-translational regulation, providing SAR-specific modes of control over autophagosome formation.
Mitophagy updates of last week 🪫🗑️
biomed.news/bims-tofagi/...
Highlights:
-two papers on the beneficial effects of mitophagy in CD8+ T cells
-VPS35 mutations in PD affect PINK1/Parkin mitophagy selectively
-review on selective autophagy initiation
Thanks to @biomednews.bsky.social for pre-sorting
