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The Shigella type III effector IpgD recodes Ca 2+ signals during invasion of epithelial cells

Abstract : The role of second messengers in the diversion of cellular processes by pathogens remains poorly studied despite their importance. Among these, Ca2+ virtually regulates all known cell processes, including cytoskeletal reorganization, inflammation, or cell death pathways. Under physiological conditions, cytosolic Ca2+ increases are transient and oscillatory, defining the so-called Ca2+ code that links cell responses to specific Ca2+ oscillatory patterns. During cell invasion, Shigella induces atypical local and global Ca2+ signals. Here, we show that by hydrolyzing phosphatidylinositol-(4,5)bisphosphate, the Shigella type III effector IpgD dampens inositol-(1,4,5)trisphosphate (InsP3) levels. By modifying InsP3 dynamics and diffusion, IpgD favors the elicitation of long-lasting local Ca2+ signals at Shigella invasion sites and converts Shigella-induced global oscillatory responses into erratic responses with atypical dynamics and amplitude. Furthermore, IpgD eventually inhibits InsP3-dependent responses during prolonged infection kinetics. IpgD thus acts as a pathogen regulator of the Ca2+ code implicated in a versatility of cell functions. Consistent with this function, IpgD prevents the Ca2+-dependent activation of calpain, thereby preserving the integrity of cell adhesion structures during the early stages of infection.
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Submitted on : Friday, October 19, 2018 - 2:29:13 PM
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Chun Hui Sun, Benjamin Wacquier, Daniel Aguilar, Nathalie Carayol, Kevin Denis, et al.. The Shigella type III effector IpgD recodes Ca 2+ signals during invasion of epithelial cells. EMBO Journal, EMBO Press, 2017, 36 (17), pp.2567 - 2580. ⟨10.15252/embj.201696272⟩. ⟨pasteur-01899400⟩

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