流感病毒M2蛋白在自噬中与LC3相关的机制.pdfVIP

Cell Host Microbe Short Article A LC3-Interacting Motif in the Influenza A Virus M2 Protein Is Required to Subvert Autophagy and Maintain Virion Stability Rupert Beale,1,2,5 Helen Wise,3,4,5 Amanda Stuart,4 Benjamin J. Ravenhill,1 Paul Digard,3,4,* and Felix Randow1,2,* 1MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK 2University of Cambridge, Department of Medicine, Addenbrooke’s Hospital, Cambridge CB2 0QQ, UK 3Roslin Institute, University of Edinburgh, Edinburgh EH25 9RG, UK 4Division of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 0QQ, UK 5These authors contributed equally to this work *Correspondence: paul.digard@roslin.ed.ac.uk (P.D.), randow@mrc-lmb.cam.ac.uk (F.R.) /10.1016/j.chom.2014.01.006 SUMMARY et al., 2009; 2012; Wild et al., 2011; Zheng et al., 2009). Binding partners of LC3/ATG8 family members typically contain an Autophagy recycles cellular components and de- LC3-interacting region (LIR). LIRs form intermolecular b sheets fends cells against intracellular pathogens. While with LC3/ATG8 family members by virtue of a consensus viruses must evade autophagocytic destruction, W/FxxI/L motif, often preceded by acidic residues (Johansen some viruses can also subvert autophagy for their and Lamark, 2011). own benefit. The ability of influenza A virus (IAV) to While autophagy restricts the growth of pathogens poorly evade autophagy depends on the Matrix 2 (M2) adapted to life in the cytosol (e.g., Salmonella enterica), profes- sional cytosol-dwelling bacteria, such as Shigella flexneri, evade ion-channel