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© Research
Publication : The EMBO journal

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

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The EMBO journal - 12 Jul 2017

Sun CH, Wacquier B, Aguilar DI, Carayol N, Denis K, Boucherie S, Valencia-Gallardo C, Simsek C, Erneux C, Lehman A, Enninga J, Arbibe L, Sansonetti P, Dupont G, Combettes L, Tran Van Nhieu G

Link to Pubmed [PMID] – 28701483

EMBO J. 2017 Sep;36(17):2567-2580

The role of second messengers in the diversion of cellular processes by pathogens remains poorly studied despite their importance. Among these, Ca(2+) virtually regulates all known cell processes, including cytoskeletal reorganization, inflammation, or cell death pathways. Under physiological conditions, cytosolic Ca(2+) increases are transient and oscillatory, defining the so-called Ca(2+) code that links cell responses to specific Ca(2+) oscillatory patterns. During cell invasion, Shigella induces atypical local and global Ca(2+) 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 Ca(2+) 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 Ca(2+) code implicated in a versatility of cell functions. Consistent with this function, IpgD prevents the Ca(2+)-dependent activation of calpain, thereby preserving the integrity of cell adhesion structures during the early stages of infection.

https://www.ncbi.nlm.nih.gov/pubmed/28701483