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. 2021 Apr 22;79(5):ftab023. doi: 10.1093/femspd/ftab023

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© The Author(s) 2021. Published by Oxford University Press on behalf of FEMS.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

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Figure 4. — GBP1 microcapsules and septin cages are complementary antimotility factors targeting S. flexneri. Actin halos around immobile S. flexneri promote the assembly of septin cages. In IFNγ-primed human epithelial cells, GBP1 forms microcapsules around both motile and immobile bacteria. These GBP1 microcapsules block IcsA-mediated actin halo and actin tail formation and supersede IcsA-dependent septin caging. Wild-type S. flexneri secretes the type III secreted effector IpaH9.8 that tags GBP1 with K48-linked ubiquitin for proteasomal degradation. The IpaH9.8-mediated evasion of GBP1-driven host defense enables S. flexneri to form actin halos and thereby renders the bacteria again susceptible for septin caging.