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Regulation of Ca2+/calmodulin kinase II inhibitor alpha (CaMKIINalpha) in virus-infected mouse brain

Sougata Saha1, Anand Ramanathan, Pundi N Rangarajan

  • 1Department of Biochemistry, Indian Institute of Science, Bangalore 560012, India.

Biochemical and Biophysical Research Communications
|October 3, 2006
PubMed

Insights

Mouse Ca(2+)/calmodulin kinase II inhibitor alpha (CaMKIINalpha) brain expression decreases during viral infections. This correlates with altered CaMKIIalpha activity, suggesting a role in Japanese encephalitis virus-induced neuropathogenesis.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Virology

Background:

  • Ca(2+)/calmodulin kinase II inhibitor alpha and beta (CaMKIINalpha/beta) inhibit Ca(2+)/calmodulin kinase II (CaMKII) in vitro.
  • The in vivo function and regulation of CaMKIINalpha/beta in the central nervous system (CNS) remain largely unknown.

Purpose of the Study:

  • To investigate the expression and regulation of CaMKIINalpha in the mouse CNS during viral infections.
  • To explore the impact of viral infection on CaMKIIalpha activity and localization.

Main Methods:

  • Analysis of CaMKIINalpha gene expression in mouse brain during Japanese encephalitis virus (JEV) and rabies virus infection.
  • Quantitative assessment of CaMKIINalpha and CaMKIINbeta mRNA levels.
  • Examination of CaMKIIalpha phosphorylation and subcellular localization.

Main Results:

  • Mouse CaMKIINalpha gene expression yields a 2.9kb brain-specific transcript.
  • CaMKIINalpha mRNA levels are significantly downregulated in the mouse brain during JEV and rabies virus infection.
  • This downregulation is specific to CaMKIINalpha, not CaMKIINbeta mRNA.
  • JEV infection induces distinct changes in CaMKIIalpha phosphorylation and subcellular localization, increasing cytosolic CaMKII activity.

Conclusions:

  • Differential regulation of CaMKIIalpha and CaMKIINalpha occurs during JEV infection.
  • These molecular changes suggest a potential role for CaMKIINalpha and CaMKIIalpha in viral pathogenesis within the CNS.

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