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Manipulation of Promyelocytic Leukemia Protein Nuclear Bodies by Marek's Disease Virus Encoded US3 Protein Kinase

Yifei Liao1, Blanca Lupiani1, Sanjay M Reddy1

  • 1Department of Veterinary Pathobiology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, TX 77843, USA.

Microorganisms
|April 3, 2021
PubMed

Insights

Marek's disease virus US3 protein kinase disrupts Promyelocytic leukemia protein nuclear bodies (PML-NBs) in chicken cells. This disruption involves a proteasome-dependent pathway, revealing a novel interaction between MDV and PML-NBs.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Promyelocytic leukemia protein nuclear bodies (PML-NBs) are key nuclear structures involved in herpesvirus replication.
  • Marek's disease virus (MDV) is an oncogenic alphaherpesvirus causing significant lymphoproliferative disease in chickens.
  • The role of MDV in regulating PML-NBs has not been previously investigated.

Purpose of the Study:

  • To investigate the role of the MDV US3 serine/threonine protein kinase in the regulation of PML-NBs.
  • To elucidate the mechanism by which MDV US3 affects PML and SP100 proteins within PML-NBs.

Main Methods:

  • Immunofluorescence assays were employed to visualize PML and SP100.
  • The kinase activity of MDV US3 was assessed for its role in disruption.
  • Proteasome inhibition using MG-132 was utilized to explore degradation pathways.

Main Results:

  • MDV US3 was found to disrupt PML and SP100 proteins in a kinase-dependent manner.
  • Treatment with MG-132 partially restored PML and SP100 levels, indicating proteasome involvement.
  • These results suggest a cellular proteasome-dependent degradation pathway is activated by MDV US3.

Conclusions:

  • This study provides the first evidence of an interaction between MDV proteins and PML-NBs.
  • MDV US3 kinase activity is crucial for the disruption of PML-NB components.
  • A proteasome-dependent mechanism underlies the MDV US3-mediated disruption of PML and SP100.
Keywords:
Marek’s disease virusPMLSP100US3protein kinase

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