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Evolution and function of bacterial RCC1 repeat effectors.

Anna Leoni Swart1, Laura Gomez-Valero2,3, Carmen Buchrieser2,3

  • 1Institute of Medical Microbiology, Faculty of Medicine, University of Zurich, Zürich, Switzerland.

Cellular Microbiology
|July 29, 2020
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Summary
This summary is machine-generated.

Intracellular bacteria like Legionella and Coxiella use unique proteins to manipulate the host cell

Keywords:
AcanthamoebaCoxiellaDictyosteliumLegionellaamoebaebacterial evolutioneffector proteinendoplasmic reticulumendosomehost-pathogen interactionmacrophagemicrotubulepathogen vacuolephosphoinositide lipidsmall GTPasetype IV secretion

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Area of Science:

  • Microbiology and Molecular Cell Biology
  • Bacterial Pathogenesis and Host-Pathogen Interactions
  • Eukaryotic Cell Signaling and Regulation

Background:

  • Intracellular bacterial pathogens possess genes with eukaryotic homologs, notably Regulator of Chromosome Condensation 1 (RCC1) repeat proteins.
  • RCC1 repeat proteins are crucial for protein-protein interactions, including the activation of the small GTPase Ran.
  • Legionella pneumophila and Coxiella burnetii, responsible for Legionnaires' disease and Q fever, encode RCC1 repeat effector proteins.

Purpose of the Study:

  • To investigate the role and mechanisms of bacterial RCC1 repeat effector proteins in manipulating host cell processes.
  • To understand how these effectors target the Ran GTPase cycle for pathogen benefit.
  • To explore the evolutionary divergence of these bacterial effectors and their cellular targets.

Main Methods:

  • Identification and characterization of RCC1 repeat effector proteins secreted by Legionella pneumophila and Coxiella burnetii.
  • Localization studies of bacterial effectors within host cells (e.g., pathogen vacuole, plasma membrane, nucleoli).
  • Analysis of effector interactions with host factors, including the Ran GTPase and its modulators, and assessment of downstream cellular effects.

Main Results:

  • Legionella pneumophila secretes effectors (LegG1, PpgA, PieG) that activate Ran GTPase, stabilize microtubules, promote vacuole motility, and enhance bacterial growth.
  • Coxiella burnetii translocates NopA to nucleoli, where it binds Ran GTPase, causing nuclear accumulation of Ran(GTP) and inhibiting NF-κB signaling.
  • Bacterial RCC1 repeat effectors target distinct components of the Ran GTPase cycle at various cellular locations.

Conclusions:

  • Bacterial pathogens have evolved diverse RCC1 repeat effectors to hijack the host Ran GTPase cycle for their survival and proliferation.
  • These effectors exhibit distinct cellular localizations and target specific elements of the Ran GTPase pathway, demonstrating divergent evolution.
  • The manipulation of the Ran GTPase cycle by bacterial effectors highlights a conserved yet adaptable strategy for intracellular pathogenesis.