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Studying RNA Interactors of Protein Kinase RNA-Activated during the Mammalian Cell Cycle
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Studying RNA Interactors of Protein Kinase RNA-Activated during the Mammalian Cell Cycle

Published on: March 5, 2019

Avian reovirus nonstructural protein p17-induced G(2)/M cell cycle arrest and host cellular protein translation

Julius L C Chulu1, Wei R Huang, L Wang

  • 1Institute of Molecular Biology, National Chung-Hsing University, Taichung, Taiwan.

Journal of Virology
|May 21, 2010
PubMed

Insights

Avian reovirus (ARV) p17 protein causes G(2)/M cell cycle arrest and shuts down host protein translation, leading to increased ARV replication. This study details the molecular pathways involved in these ARV-induced cellular disruptions.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Avian reovirus (ARV) is an important poultry pathogen.
  • Understanding ARV's interaction with host cells is crucial for disease control.

Purpose of the Study:

  • To investigate the effects of ARV p17 protein on host cell cycle progression.
  • To elucidate the role of p17 in ARV-induced host protein translation shutoff.
  • To determine how these cellular events impact viral replication.

Main Methods:

  • ARV infection and p17 protein transfection in cell cultures.
  • Cell cycle analysis using flow cytometry.
  • Western blotting to detect protein phosphorylation and expression levels.
  • Inhibition of mTOR pathway using rapamycin.

Main Results:

  • ARV infection and p17 transfection induced G(2)/M cell cycle arrest.
  • p17 upregulated and phosphorylated key cell cycle regulatory proteins (ATM, p53, p21, Cdc2, cyclin B1, Chk1, Chk2, Cdc25C).
  • p17 suppressed host protein translation by inhibiting initiation and elongation factors (eEF2, eIF2α, eIF4E, eIF4B, eIF4G, 4E-BP1, Mnk-1).
  • G(2)/M arrest and translation shutoff correlated with increased ARV replication.
  • Inhibition of cap-dependent translation did not affect ARV replication.

Conclusions:

  • ARV p17 protein is responsible for inducing G(2)/M cell cycle arrest and host protein translation shutoff.
  • These p17-mediated cellular disruptions enhance ARV replication.
  • ARV replication is not dependent on cap-dependent translation pathways targeted by p17.

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