Journal
EMBO JOURNAL
Volume 37, Issue 4, Pages -Publisher
WILEY
DOI: 10.15252/embj.201797840
Keywords
autophagy; phagocytosis; LC3; ATG16L1; influenza
Categories
Funding
- Cambridge NIHR BRC Cell Phenotyping Hub
- Cancer Research UK [C47718/A16337]
- Medical Research Council [RG89611]
- BBSRC Institute Strategic Programme Gut Health and Food Safety [BB/J004529/1]
- Biotechnology and Biological Sciences Research Council [BB/R009988/1, BBS/E/F/000PR10353, BBS/E/B/000C0434, BBS/E/F/000PR10355] Funding Source: researchfish
- Cancer Research UK [16337] Funding Source: researchfish
- Medical Research Council [MR/M00869X/1] Funding Source: researchfish
- BBSRC [BBS/E/F/000PR10355, BBS/E/F/000PR10353, BBS/E/B/000C0434] Funding Source: UKRI
- MRC [MR/M00869X/1] Funding Source: UKRI
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A hallmark of macroautophagy is the covalent lipidation of LC3 and insertion into the double-membrane phagophore, which is driven by the ATG16L1/ATG5-ATG12 complex. In contrast, non-canonical autophagy is a pathway through which LC3 is lipidated and inserted into single membranes, particularly endolysosomal vacuoles during cell engulfment events such as LC3-associated phagocytosis. Factors controlling the targeting of ATG16L1 to phagophores are dispensable for non-canonical autophagy, for which the mechanism of ATG16L1 recruitment is unknown. Here we show that the WD repeat-containing C-terminal domain (WD40 CTD) of ATG16L1 is essential for LC3 recruitment to endolysosomal membranes during non-canonical autophagy, but dispensable for canonical autophagy. Using this strategy to inhibit non-canonical autophagy specifically, we show a reduction of MHC class II antigen presentation in dendritic cells from mice lacking the WD40 CTD. Further, we demonstrate activation of non-canonical autophagy dependent on the WD40 CTD during influenza A virus infection. This suggests dependence on WD40 CTD distinguishes between macroautophagy and non-canonical use of autophagy machinery.
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