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Glial cell type-specific subcellular localization of 14-3-3 zeta: an implication for JCV tropism

Shivani Lamba1, Veerasamy Ravichandran, Eugene O Major

  • 1Laboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1296, USA.

Glia
|December 9, 2008
PubMed

Insights

14-3-3 zeta protein accumulates in the nucleus of cells infected with JC virus (JCV), suggesting its role in progressive multifocal leukoencephalopathy (PML) pathogenesis. This nuclear presence may influence JCV susceptibility.

Area of Science:

  • Neuroscience
  • Virology
  • Cell Biology

Background:

  • 14-3-3 proteins are implicated in various cellular functions.
  • Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease caused by JC virus (JCV).
  • 14-3-3 isoforms accumulate in glial cells in PML patient brains, but their role in JCV infection is unknown.

Purpose of the Study:

  • To investigate the relationship between 14-3-3 isoforms and JCV infection in vitro.
  • To examine the cellular localization of 14-3-3 isoforms in neural progenitors and astrocytes.
  • To determine if 14-3-3 zeta influences JCV susceptibility.

Main Methods:

  • Localization studies of six 14-3-3 isoforms in human neural progenitors and progenitor-derived astrocytes (PDAs).
  • Analysis of 14-3-3 zeta localization in cells with and without JCV exposure.
  • Assessment of 14-3-3 zeta levels and localization following TGF-beta1 treatment.

Main Results:

  • 14-3-3 zeta translocated to the nucleus during progenitor differentiation into PDAs.
  • JCV infection induced nuclear localization of 14-3-3 zeta in progenitor cells.
  • JCV-infected PDAs showed elevated 14-3-3 zeta levels.
  • TGF-beta1 increased JCV infection and 14-3-3 zeta nuclear presence.

Conclusions:

  • Nuclear presence of 14-3-3 zeta may be crucial for JCV infection.
  • 14-3-3 zeta isoform may determine cellular susceptibility to JCV.
  • Further research into 14-3-3 zeta's role in PML pathogenesis is warranted.

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