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Functional interactions between polydnavirus and host cellular innexins.

N K Marziano1, D K Hasegawa, P Phelan

  • 1School of Biosciences, University of Kent, Canterbury, Kent, UK.

Journal of Virology
|August 5, 2011
PubMed
Summary
This summary is machine-generated.

Polydnaviruses, like Campoletis sonorensis ichnovirus (CsIV), alter caterpillar physiology. CsIV vinnexins form functional gap junctions, potentially causing cellular pathologies by altering intercellular communication.

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Area of Science:

  • Virology
  • Molecular Biology
  • Insect Pathology

Background:

  • Polydnaviruses are double-stranded DNA viruses transmitted by parasitoid wasps.
  • These viruses infect host caterpillars, causing physiological disruptions through gene expression.
  • The Campoletis sonorensis ichnovirus (CsIV) encodes four innexin homologues, termed vinnexins.

Purpose of the Study:

  • To investigate the functionality of CsIV vinnexinQ1 and vinnexinQ2 in forming gap junctions.
  • To examine the interactions between CsIV vinnexins and the host caterpillar's Innexin2.
  • To determine if vinnexin-Innexin2 interactions alter gap junctional communication.

Main Methods:

  • Expression of vinnexinQ1 and vinnexinQ2 in paired Xenopus oocytes to assess junction formation.
  • Co-expression of vinnexins with Spodoptera frugiperda Innexin2 in cell pairs.
  • Functional analysis of gap junctions formed by vinnexins alone, Innexin2 alone, or in combination.

Main Results:

  • VinnexinQ1 and vinnexinQ2 form functional gap junctions in a heterologous system.
  • Vinnexins interact differentially with the insect Innexin2 orthologue.
  • Co-expression of vinnexins and Innexin2 results in functional junctions with distinct properties compared to Innexin2 alone.

Conclusions:

  • CsIV vinnexins are functional gap junction proteins.
  • Altered gap junctional intercellular communication due to vinnexin-Innexin2 interactions may contribute to ichnovirus-induced cellular pathologies in caterpillars.