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Phosphoinositides and PIPs

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Related Experiment Video

Updated: Jun 16, 2026

Identification of Inositol Phosphate or Phosphoinositide Interacting Proteins by Affinity Chromatography Coupled to Western Blot or Mass Spectrometry
08:07

Identification of Inositol Phosphate or Phosphoinositide Interacting Proteins by Affinity Chromatography Coupled to Western Blot or Mass Spectrometry

Published on: July 26, 2019

Phosphoinositides influence pathogen surfing: EPEC rights the SHIP.

Kenneth G Campellone1

  • 1Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA. campellone@berkeley.edu

Cell Host & Microbe
|February 2, 2010
PubMed
Summary
This summary is machine-generated.

Enteropathogenic E. coli (EPEC) uses the translocated effector protein Tir to create actin pedestals. New findings reveal Tir recruits SHIP2 phosphatase, stabilizing these bacterial adhesion structures via a PI(3,4)P2-enriched membrane platform.

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Fluorescence-Based Measurements of Phosphatidylserine/Phosphatidylinositol 4-Phosphate Exchange Between Membranes
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Identification of Inositol Phosphate or Phosphoinositide Interacting Proteins by Affinity Chromatography Coupled to Western Blot or Mass Spectrometry
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Fluorescence-Based Measurements of Phosphatidylserine/Phosphatidylinositol 4-Phosphate Exchange Between Membranes
08:49

Fluorescence-Based Measurements of Phosphatidylserine/Phosphatidylinositol 4-Phosphate Exchange Between Membranes

Published on: March 14, 2021

Area of Science:

  • Microbiology
  • Cell Biology
  • Molecular Biology

Background:

  • Enteropathogenic E. coli (EPEC) injects the translocated intimin receptor (Tir) into host cells.
  • Tir is crucial for EPEC pathogenesis, inducing actin polymerization and the formation of characteristic actin pedestals on the host cell surface.
  • The initial signaling events mediated by Tir, involving phosphotyrosines, are known to trigger actin assembly.

Purpose of the Study:

  • To investigate the role of additional tyrosine residues in Tir beyond the initial signaling sites.
  • To identify host cell factors recruited by Tir that contribute to pedestal stabilization.
  • To elucidate the molecular mechanism by which Tir stabilizes actin pedestals.

Main Methods:

  • Site-directed mutagenesis of Tir to alter specific tyrosine residues.
  • Co-immunoprecipitation assays to identify interacting proteins.
  • Immunofluorescence microscopy to visualize actin pedestal formation and localization of proteins.
  • Lipid-binding assays and mass spectrometry to analyze phosphoinositide enrichment.

Main Results:

  • Two previously uncharacterized tyrosines in Tir were identified as critical for recruiting the inositol phosphatase SHIP2.
  • Recruitment of SHIP2 by Tir leads to the localized generation of phosphatidylinositol 3,4-bisphosphate (PI(3,4)P2).
  • This PI(3,4)P2-enriched membrane microdomain acts as a platform that enhances the stability of actin pedestals.

Conclusions:

  • Tir employs a dual mechanism involving initial phosphotyrosines for actin polymerization and additional tyrosines for SHIP2 recruitment.
  • SHIP2-mediated PI(3,4)P2 generation is essential for stabilizing the actin pedestal structure, a key virulence factor of EPEC.
  • This study reveals a novel host-pathogen interaction critical for bacterial adhesion and colonization.