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Shigella flexneri evades septin-mediated cell-autonomous immunity via protein ADP-riboxanation

ABSTRACT: We demonstrate that OspC effectors enable S. flexneri to evade septin cage entrapment. Mechanistically, OspC catalyzes ADP-riboxanation of SEPT9 at Arg561, a critical site essential for stabilizing septin hetero-oligomers. Notably, ADP-riboxanation or mutation of Arg561 impairs septin polymerization and hence the assembly of higher-order structures, including filaments and cage-like structures. Finally, we provide evidence that S. flexneri OspC effectors act synergistically with OspG to antagonize septin cage entrapment via two distinct post-translational modifications.

ORGANISM(S): Homo Sapiens

SUBMITTER: Xiaoyun Liu

PROVIDER: PXD070327 | iProX | Tue Nov 04 00:00:00 GMT 2025

REPOSITORIES: iProX

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Shigella flexneri evades septin-mediated cell-autonomous immunity via protein ADP-riboxanation.

Tang Zhiheng Z Xian Wei W Özbaykal Güler Gizem G Zhang Hanyu H Wang Ying Y Zhan Naizheng N Liu Huwei H You Fuping F Zou Qinghua Q Mostowy Serge S Liu Xiaoyun X

Nature communications 20260127 1

Cell-autonomous immunity represents evolutionarily conserved defense mechanisms present in both immune and non-immune cells. One of such mechanisms is mediated by cytoskeletal septins that entrap cytosolic bacterial pathogens within cage-like structures. To promote infection, Shigella flexneri delivers effector proteins directly into host cells via a type III secretion system. Here we demonstrate that OspC effectors enable Shigella flexneri to evade septin cage entrapment. Mechanistically, OspC ...[more]

PMID: 41593083

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