Conversion of PtdIns(4, 5)P2 into PtdIns(5)P by the S.flexneri effector IpgD reorganizes host cell morphology

Kirsten Niebuhr, Sylvie Giuriato, Thierry Pedron, Dana J. Philpott, Frédérique Gaits, Julia Sable, Michael P. Sheetz, Claude Parsot, Philippe J. Sansonetti, Bernard Payrastre

Research output: Contribution to journalArticlepeer-review

242 Scopus citations


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)P2] into phosphatidylinositol 5-monophosphate [PtdIns(5)P] that then accumulates. Transfection experiments indicate that the transformation of PtdIns(4, 5)P2 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.

Original languageEnglish (US)
Pages (from-to)5069-5078
Number of pages10
JournalEMBO Journal
Issue number19
StatePublished - Oct 1 2002
Externally publishedYes


  • Bacterial entry
  • IpgD
  • Phosphoinositides
  • S.flexneri

ASJC Scopus subject areas

  • General Neuroscience
  • Molecular Biology
  • General Biochemistry, Genetics and Molecular Biology
  • General Immunology and Microbiology


Dive into the research topics of 'Conversion of PtdIns(4, 5)P2 into PtdIns(5)P by the S.flexneri effector IpgD reorganizes host cell morphology'. Together they form a unique fingerprint.

Cite this