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Title: Virus Innexins induce alterations in insect cell and tissue function

Author
item Hasegawa, Daniel
item ERICKSON, STEPHANIE - Clemson University
item HERSH, BRADLEY - Allegheny College
item TURNBULL, MATTHEW - Clemson University

Submitted to: Journal of Insect Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/9/2017
Publication Date: N/A
Citation: N/A

Interpretive Summary: Natural parasitism by parasitoid wasps is an important means of insect biocontrol. Polydnaviruses are a group of insect viruses that have a symbiotic relationship with parasitoid wasps, which may be used as a biocontrol agent for insect pests. During insect parasitization, polydnaviruses injected by the wasp into a host caterpillar leads to immune suppression and developmental arrest. Here, we studied a polydnavirus gene family to understand its roles in insect parasitism during the senior author's PhD study at Clemson University. We found that the expression of several members of the polydnavirus gene family disrupt host insect cell shape, as well as affect molecule trafficking between adjacent cells. Furthermore, expression of one of the genes in the model insect, fruit fly, resulted in developmental arrest and mortality. These data support the roles for involvement of polydnavirus genes in wasp parasitism and polydnavirus infection. Overall, these data contribute to our understanding in the mechanism of wasp parasitism of insect hosts, which is fundamental in devising a novel and effective biocontrol strategy to manage agricultural insect pests.

Technical Abstract: Polydnaviruses 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 of 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.