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JC Virus Agnogene Regulates Histone-Modifying Enzymes via PML-NBs: Transcriptomics in VLP-Expressing Cells.

Yukiko Shishido-Hara1, Takeshi Yaoi2

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The JC virus (JCV) agnogene influences epigenetic regulation within glial cells, affecting cell cycle control. This occurs in promyelocytic leukemia nuclear bodies (PML-NBs) during virus-like particle assembly.

Keywords:
JC virus (JCV)agnogenecapsid proteinschromatin dynamicshistone modificationpromyelocytic leukemia (PML)promyelocytic leukemia nuclear bodies (PML-NBs)virus-like particles (VLPs)

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Area of Science:

  • Neurovirology
  • Molecular Biology
  • Epigenetics

Background:

  • JC virus (JCV) infects glial cells, causing progressive multifocal leukoencephalopathy.
  • JCV has a double-stranded DNA genome with early and late coding regions and a control region.
  • Capsid proteins assemble into virus-like particles (VLPs) within promyelocytic leukemia nuclear bodies (PML-NBs).

Purpose of the Study:

  • To investigate the function of the JCV agnogene.
  • To determine the agnogene's role in VLP formation and its impact on host cell gene expression.
  • To explore the agnogene's influence on epigenetic regulation and cell cycle control.

Main Methods:

  • Cell culture systems for VLP formation with and without the agnogene.
  • Microarray analysis for differential gene expression.
  • Analysis of histone-modifying enzymes, kinases, and phosphatases.
  • Examination of JCV-infected human brain tissue.

Main Results:

  • The JCV agnogene significantly altered the expression of histone-modifying enzymes (EHMT1, PRMT7, KDM2B, KDM5C, KDM6B) and kinases/phosphatases.
  • CTDP1, involved in RNA polymerase II regulation, was also differentially expressed.
  • Changes in gene expression were more pronounced in the presence of the agnogene.
  • JCV-infected glial cells in human brain tissue maintained a diploid chromosomal complement, suggesting G2 arrest.

Conclusions:

  • The JCV agnogene likely influences epigenetic regulation associated with PML-NBs.
  • This epigenetic modulation may impact cell cycle control in infected glial cells.
  • The precise mechanism of G2 arrest in JCV-infected cells requires further elucidation.