%0 Journal Article %T ATP-mediated Erk1/2 activation stimulates bacterial capture by filopodia, which precedes Shigella invasion of epithelial cells. %+ Centre interdisciplinaire de recherche en biologie (CIRB) %+ Centre National de la Recherche Scientifique (CNRS) %+ Pathogénie Microbienne Moléculaire %+ Microscopie Ultrastructurale (Plate-forme) %+ Collège de France - Chaire Microbiologie et Maladies infectieuses %A Romero, Stéphane %A Grompone, Gianfranco %A Carayol, Nathalie %A Mounier, Joëlle %A Guadagnini, Stéphanie %A Prevost, Marie-Christine %A Sansonetti, Philippe %A van Nhieu, Guy Tran %Z This work was supported by the Institut National de la Sante et de la Recherche Medicale, the Institut Pasteur, the Institut National pour la Recherche Agronomique, the College de France, Agence Nationale pour la Recherche grants and National Institute of Health grant AI067949. P.J.S. is a Howard Hughes Medical Institute foreign scholar. S.R. received a fellowship from the Fondation pour la Recherche Medicale. %< avec comité de lecture %@ 1931-3128 %J Cell Host and Microbe %I Elsevier %V 9 %N 6 %P 508-19 %8 2011-06-16 %D 2011 %R 10.1016/j.chom.2011.05.005 %M 21669399 %Z Life Sciences [q-bio]/Cellular Biology %Z Life Sciences [q-bio]/Microbiology and ParasitologyJournal articles %X Shigella, the causative agent of bacillary dysentery in humans, invades epithelial cells, using a type III secretory system (T3SS) to inject bacterial effectors into host cells and remodel the actin cytoskeleton. ATP released through connexin hemichanels on the epithelial membrane stimulates Shigella invasion and dissemination in epithelial cells. Here, we show that prior to contact with the cell body, Shigella is captured by nanometer-thin micropodial extensions (NMEs) at a distance from the cell surface, in a process involving the T3SS tip complex proteins and stimulated by ATP- and connexin-mediated signaling. Upon bacterial contact, NMEs retract, bringing bacteria in contact with the cell body, where invasion occurs. ATP stimulates Erk1/2 activation, which controls actin retrograde flow in NMEs and their retraction. These findings reveal previously unappreciated facets of interaction of an invasive bacterium with host cells and a prominent role for Erk1/2 in the control of filopodial dynamics. %G English %L pasteur-00685251 %U https://riip.hal.science/pasteur-00685251 %~ PASTEUR %~ RIIP %~ ENS-PARIS %~ ESPCI %~ CNRS %~ CDF %~ RIIP_PARIS %~ PARISTECH %~ PSL %~ ENS-PSL %~ ESPCI-PSL %~ CDF-PSL %~ FRM