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Conversion of PtdIns(4,5)P 2 into PtdIns(5)P by the S.flexneri effector IpgD reorganizes host cell morphology
Author(s) -
Niebuhr Kirsten,
Giuriato Sylvie,
Pedron Thierry,
Philpott Dana J.,
Gaits Frédérique,
Sable Julia,
Sheetz Michael P.,
Parsot Claude,
Sansonetti Philippe J.,
Payrastre Bernard
Publication year - 2002
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/cdf522
Subject(s) - biology , effector , morphology (biology) , microbiology and biotechnology , host (biology) , genetics
Phosphoinositides play a central role in the control of several cellular events including actin cytoskeleton organization. Here we show that, upon infection of epithelial cells with the Gram‐negative pathogen Shigella flexneri , the virulence factor IpgD is translocated directly into eukaryotic cells and acts as a potent inositol 4‐phosphatase that specifically dephosphorylates phosphatidylinositol 4,5‐bisphosphate [PtdIns(4,5)P 2 ] into phosphatidylinositol 5‐monophosphate [PtdIns(5)P] that then accumulates. Transfection experiments indicate that the transformation of PtdIns(4,5)P 2 into PtdIns(5)P by IpgD is responsible for dramatic morphological changes of the host cell, leading to a decrease in membrane tether force associated with membrane blebbing and actin filament remodelling. These data provide the molecular basis for a new mechanism employed by a pathogenic bacterium to promote membrane ruffling at the entry site.