ArticleAutophagy2026
Hijacking a cellular highway: non-lipidated LC3 proteins and PCNT (pericentrin) drive influenza a virus uncoating.
Article in Autophagy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
MAP1LC3/LC3 (microtubule associated protein 1 light chain 3) proteins have long been thought to carry out their cellular and organismal functions, including macroautophagy/autophagy, exclusively in their lipidated form, also referred to as Atg8ylation. They are anchored mainly to the phosphatidylethanolamine present in membranes through the action of two ubiquitin-like conjugation systems. Our recent work, however, uncovered a role of non-lipidated LC3s during influenza A virus (IAV) infection. We revealed that LC3s, together with the centrosomal scaffold protein PCNT (pericentrin), form a dynein adaptor complex that facilitates IAV uncoating at late endosomes (LEs). We also showed that co-opting the LC3s-PCNT complex is an alternative strategy to aggresome processing machinery (APM) hijacking via HDAC6, allowing IAV to exploit the force generated by dynein-dependent motors for virion uncoating and genome delivery in the host cytoplasm. Notably, the function of LC3s in IAV uncoating does not require their Atg8ylation or the core autophagy machinery, and PCNT's role is independent from its centrosomal localization. These findings redefine LC3s as multifunctional adaptor proteins and reveal how viruses can co-opt centrosome assembly machinery components for host invasion.
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