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Updated: Jul 29, 2025

Single Cell Measurements of Vacuolar Rupture Caused by Intracellular Pathogens
10:39

Single Cell Measurements of Vacuolar Rupture Caused by Intracellular Pathogens

Published on: June 12, 2013

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Pathogen vacuole membrane contact sites - close encounters of the fifth kind

Simone Vormittag1, Rachel J Ende2, Isabelle Derré2

  • 1Institute of Medical Microbiology, University of Zürich, Gloriastrasse 30, 8006 Zürich, Switzerland.

Microlife
|May 24, 2023
PubMed

Insights

Membrane contact sites (MCS) mediate short-range organelle communication. Bacterial pathogens hijack MCS lipid transfer components for intracellular survival and replication.

Area of Science:

  • Cell Biology
  • Microbiology
  • Molecular Biology

Background:

  • Vesicular trafficking is a well-understood mechanism for long-range intracellular delivery.
  • Membrane contact sites (MCS) facilitate short-range (10-30 nm) communication between organelles and pathogen vacuoles.
  • MCS are critical for non-vesicular transport of small molecules like lipids and calcium.

Purpose of the Study:

  • To review the role of MCS components in intracellular pathogen survival.
  • To elucidate how bacterial pathogens subvert MCS for their own benefit.

Main Methods:

  • Literature review of studies on MCS components and pathogen interactions.
  • Analysis of effector proteins secreted by bacterial pathogens.
  • Discussion of key MCS lipid transfer proteins: VAP, OSBPs, CERT, Sac1, and PtdIns(4)P.

Main Results:

  • MCS components, including VAP, OSBPs, CERT, Sac1, and PtdIns(4)P, are crucial for lipid transfer.
  • Bacterial pathogens and their secreted effectors actively manipulate these MCS components.
  • This manipulation aids pathogens in intracellular survival and replication within host cells.

Conclusions:

  • Membrane contact sites are essential for intracellular pathogen strategies.
  • Targeting MCS components represents a significant mechanism for bacterial pathogenesis.
  • Understanding MCS-pathogen interactions can reveal novel therapeutic targets.
Keywords:
ChlamydiaCoxiellaDictyostelium discoideumFFAT motifLegionellaLegionnaires’ diseaseSac1 phosphoinositide phosphataseSalmonellaVAPendoplasmic reticulumlipid transfer proteinsmembrane contact siteoxysterol binding proteinspathogen vacuolephosphoinositide

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