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dc.contributor.authorHasegawa, Daniel K.
dc.contributor.authorErickson, Stephanie L.
dc.contributor.authorHersh, Bradley M.
dc.contributor.authorTurnbull, Matthew W.
dc.date.accessioned2017-01-26T19:28:19Z
dc.date.available2017-01-26T19:28:19Z
dc.date.issued2017-01-07
dc.identifier.citationHasegawa, D.K., et al. (2017). Virus Innexins induce alterations in insect cell and tissue function. Journal of Insect Physiology 98: 173-181. doi:10.1016/j.jinsphys.2017.01.003en_US
dc.identifier.issn0022-1910
dc.identifier.urihttp://hdl.handle.net/10456/42339
dc.description.abstractPolydnaviruses are dsDNA viruses that induce immune and developmental alterations in their caterpillar hosts. Characterization of polydnavirus gene families and family members is necessary to understand mechanisms of pathology and evolution of these viruses, and may aid to elucidate the role of host homologues if present. For example, the polydnavirus vinnexin gene family encodes homologues of insect gap junction genes (innexins) that are expressed in host immune cells (hemocytes). While the roles of Innexin proteins and gap junctions in insect immunity are largely unclear, we previously demonstrated that Vinnexins form functional gap junctions and alter the junctional characteristics of a host Innexin when co-expressed in paired Xenopus oocytes. Here, we test the effect of ectopic vinnexin expression on host cell physiology using both a lepidopteran cell culture model and a dipteran whole organism model. Vinnexin expression in the cell culture system resulted in gene-specific alterations in cell morphology and a slight, but non-statistically significant, reduction in gap junction activity as measured by dye transfer, while ectopic expression of a lepidopteran innexin2 gene led to morphological alterations and increase in gap junction activity. Global ectopic expression in the model dipteran, Drosophila melanogaster, of one vinnexin (vinnexinG) or D. melanogaster innexin2 (Dm-inx2) resulted in embryonic lethality, while expression of the other vinnexin genes had no effect. Furthermore, ectopic expression of vinnexinG, but not other vinnexin genes or Dm-inx2, in D. melanogaster larval gut resulted in developmental arrest in the pupal stage. These data indicate the vinnexins likely have gene-specific roles in host manipulation. They also support the use of Drosophila in further analysis of the role of Vinnexins and other polydnavirus genes in modifying host physiological processes. Finally, our findings suggest the vinnexin genes may be useful to perturb and characterize the physiological functions of insect Innexins.en_US
dc.language.isoen_USen_US
dc.publisherElsevieren_US
dc.relation.ispartofJournal of Insect Physiologyen_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.jinsphys.2017.01.003en_US
dc.rightsThis article has an embargo and can only be accessed through the publisher's website.en_US
dc.subjectGap junctionen_US
dc.subjectHemocytic encapsulationen_US
dc.subjectInnexinen_US
dc.subjectPolydnavirusen_US
dc.subjectVinnexinen_US
dc.titleVirus Innexins induce alterations in insect cell and tissue functionen_US
dc.description.versionPublished articleen_US
dc.contributor.departmentBiologyen_US
dc.citation.volume98en_US
dc.citation.issue1en_US
dc.citation.spage173en_US
dc.citation.epage181en_US
dc.identifier.doi10.1016/j.jinsphys.2017.01.003
dc.contributor.avlauthorHersh, Bradley M.


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