The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
A Bacterial Effector Reveals the V-ATPase-ATG16L1 Axis that Initiates Xenophagy
Open accessAbstract
Antibacterial autophagy (xenophagy) is an important host defense, but how it is initiated is unclear. Here, we performed a bacterial transposon screen and identified a T3SS effector SopF that potently blocked Salmonella autophagy. SopF was a general xenophagy inhibitor without affecting canonical autophagy. S. Typhimurium ΔsopF resembled S. flexneri ΔvirAΔicsB with the majority of intracellular bacteria targeted by autophagy, permitting a CRISPR screen that identified host V-ATPase as an essential factor. Upon bacteria-caused vacuolar damage, the V-ATPase recruited ATG16L1 onto bacteria-containing vacuole, which was blocked by SopF. Mammalian ATG16L1 bears a WD40 domain required for interacting with the V-ATPase. Inhibiting autophagy by SopF promoted S. Typhimurium proliferation in vivo. SopF targeted Gln124 of ATP6V0C in the V-ATPase for ADP-ribosylation. Mutation of Gln124 also blocked xenophagy, but not canonical autophagy. Thus, the discovery of SopF reveals the V-ATPase-ATG16L1 axis that critically mediates autophagic recognition of intracellular pathogen.
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1 retracted
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Metadata
- Authors
- Xu, Y., Zhou, P., Cheng, S., Lu, Q., Nowak, K., Hopp, A.-K., Li, L., Shi, X., Zhou, Z., Gao, W., Li, D., He, H., Liu, X., Ding, J., Hottiger, M. O., & Shao, F.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2019-07
- Volume
- 178
- Issue
- 3
- Pages
- 552-566.e20
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2961013416
- Cited by
- 361
- References
- 61
- FWCI
- 23.85
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Xu, Y., Zhou, P., Cheng, S., Lu, Q., Nowak, K., Hopp, A.-K., Li, L., Shi, X., Zhou, Z., Gao, W., Li, D., He, H., Liu, X., Ding, J., Hottiger, M. O., & Shao, F. (2019). A Bacterial Effector Reveals the V-ATPase-ATG16L1 Axis that Initiates Xenophagy. Cell. https://doi.org/10.1016/j.cell.2019.06.007
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