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Gap Junctions in the Mosquito, Aedes aegypti

Calkins, Travis L
http://orcid.org/0000-0002-9820-1294
http://rave.ohiolink.edu/etdc/view?acc_num=osu149217328492135

Abstract Details

2017, Doctor of Philosophy, Ohio State University, Entomology.
Mosquitoes are the most dangerous animals on the planet due to the pathogens they transmit to humans. The yellow fever mosquito, Aedes aegypti, is the study organism of this dissertation, as well as the primary vector for the viruses that cause yellow, dengue, chikungunya, and Zika fevers in humans. Unfortunately, many of these diseases lack effective vaccinations and/or therapeutics and instead must be prevented through control of the mosquito vector. Our current approach to mosquito control relies primarily on the use of insecticides to suppress mosquito populations. While these chemicals are incredibly effective at killing mosquitoes, they also exert a strong selective pressure driving the evolution of resistance. In order to combat this resistance, current compounds must be modified and new targets need to be identified. In this dissertation I focus on the latter with mosquito gap junctions as my potential targets of interest. Gap junctions are intercellular channels that mediate direct communication between adjacent cells via the transfer of small molecules and/or ions. Gap junctions are formed by protein subunits known as connexins in vertebrates and innexins in invertebrates, which are evolutionarily distinct sharing no significant amino acid homology. Despite their distinct evolutionary origins, both connexin and innexin formed gap junctions play integral roles in processes from embryogenesis to reproduction. Here I expand the knowledge base of mosquito gap junctions through examination of gene expression, iii protein localization, pharmacological inhibition, and RNAi based gene knockdown. I find that gap junction inhibitors kill and incapacitate larval and adult female mosquitoes, and inhibit diuresis in adult females. Moreover, RNAi to knockdown the mRNA expression of innexin genes decreases survival. Additionally, I show splice variation for 2 innexin mRNAs, describe innexin gene expression throughout the animal, localize the inx3 protein, and characterize changes in innexin gene expression after a blood meal. Finally, I demonstrate the involvement of innexins in crop muscle contractions and the potential cell signaling mechanism that leads to the opening or closure of gap junctions in the crop musculature. Taken together this work sets a strong foundation for future investigations of gap junctions in the mosquito and suggests that gap junctions may provide targets for the development of novel insecticides.
Peter Piermarini, Ph.D. (Advisor)
Denlinger David, Ph.D. (Committee Member)
Anelli Carol, Ph.D. (Committee Member)
Reed Johnson, Ph.D. (Committee Member)
178 p.
Entomology
Gap Junctions; Innexins; Mosquitoes; qPCR; Immunohistochemistry; Pharmacology

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Citations

  • Calkins, T. L. (2017). Gap Junctions in the Mosquito, Aedes aegypti [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu149217328492135

    APA Style (7th edition)

  • Calkins, Travis. Gap Junctions in the Mosquito, Aedes aegypti. 2017. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu149217328492135.

    MLA Style (8th edition)

  • Calkins, Travis. "Gap Junctions in the Mosquito, Aedes aegypti." Doctoral dissertation, Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu149217328492135

    Chicago Manual of Style (17th edition)

osu149217328492135
533
© 2017, all rights reserved.
This open access ETD is published by The Ohio State University and OhioLINK.