{"id":{"repo_id":"arizona-thes","oai_identifier":"oai:repository.arizona.edu:10150/628409"},"canonical_url":"https://search.dev.ndltd.org/etd/arizona-thes/oai:repository.arizona.edu:10150/628409","repository":{"repo_id":"arizona-thes","name":"University of Arizona","base_url":"https://repository.arizona.edu/oai/request"},"display":{"title":"Genetically Modifying Mosquitoes Without Compromising Fitness: Can It Be Done?","abstract":"Malaria is a mosquito-borne disease caused by parasites belonging to the genus Plasmodium. Malaria remains one of the most devastating infectious diseases, killing nearly half a million people each year (WHO 2015). 1,2 With the current increase in drug and insecticide resistance, there is an urgent need to develop novel strategies for malaria control. One such strategy to genetically engineer mosquito vectors to make them resistant to infection by malaria parasites in order to replace the wild population with malaria refractory mosquitoes. The insulin/IGF-like signaling (IIS) pathway is one potential target for a population replacement strategy since it regulates metabolism, immunity, lifespan and reproduction in mosquitoes. We previously generated a transgenic Anopheles stephensi line with increased insulin signaling in the fat body. Surprisingly, these transgenic mosquitoes survived significantly longer than their non-transgenic siblings, while in nearly every other organism increased IIS resulted in a decrease in lifespan. In this work, we sought to define how the fat body IIS controls lifespan, and also to determine the impact of the fat body IIS on reproduction, metabolism, and Plasmodium resistance. We found that overexpression of the molecule Akt, a key IIS nexus molecule, resulted in an increased overall fitness and enhanced Plasmodium falciparum parasite resistance in transgenic Anopheles stephensi, as compared to their non-transgenic siblings. Overall results from these studies highlight the important role of IIS in the mosquito fat body in controlling lifespan, reproduction, metabolism and immunity.","abstract_html":"Malaria is a mosquito-borne disease caused by parasites belonging to the genus Plasmodium. Malaria remains one of the most devastating infectious diseases, killing nearly half a million people each year (WHO 2015). 1,2 With the current increase in drug and insecticide resistance, there is an urgent need to develop novel strategies for malaria control. One such strategy to genetically engineer mosquito vectors to make them resistant to infection by malaria parasites in order to replace the wild population with malaria refractory mosquitoes. The insulin/IGF-like signaling (IIS) pathway is one potential target for a population replacement strategy since it regulates metabolism, immunity, lifespan and reproduction in mosquitoes. We previously generated a transgenic Anopheles stephensi line with increased insulin signaling in the fat body. Surprisingly, these transgenic mosquitoes survived significantly longer than their non-transgenic siblings, while in nearly every other organism increased IIS resulted in a decrease in lifespan. In this work, we sought to define how the fat body IIS controls lifespan, and also to determine the impact of the fat body IIS on reproduction, metabolism, and Plasmodium resistance. We found that overexpression of the molecule Akt, a key IIS nexus molecule, resulted in an increased overall fitness and enhanced Plasmodium falciparum parasite resistance in transgenic Anopheles stephensi, as compared to their non-transgenic siblings. Overall results from these studies highlight the important role of IIS in the mosquito fat body in controlling lifespan, reproduction, metabolism and immunity.","abstract_has_math":false,"creators":["Hun, Lewis Vibul"],"institution":"The University of Arizona.","degree_name":"Ph.D.","degree_level":"doctoral","degree_discipline":"Graduate College","degree_department":null,"school":null,"contributors":[],"advisors":["Riehle, Michael A."],"committee_chairs":[],"committee_members":["Walker, Kathleen R.","Miesfeld, Rorger L.","Jewett, John C."],"year":2018,"date_issued":"2018","date_published":"2018","updated_at":"2026-07-24T00:55:10Z","subjects":["Anopheles stephensi","Lifespan and reproduction","Mosquito immunity","Mosquito insulin-like peptides","Mosquito metabolism","Transgenic mosquito"],"languages":["en"],"rights":["Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction, presentation (such as public display or performance) of protected items is prohibited except with permission of the author."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10150/628409","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Riehle, Michael A."]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Walker, Kathleen R.","Miesfeld, Rorger L.","Jewett, John C."]},{"key":"dc:creator","label":"Author","values":["Hun, Lewis Vibul"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2018-08-09T20:15:35Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2018-08-09T20:15:35Z"]},{"key":"dc:date.issued","label":"Date","values":["2018"]},{"key":"dc:publisher","label":"Institution","values":["The University of Arizona."]},{"key":"dc:type","label":"Dc Type","values":["text","Electronic Dissertation"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Graduate College","Entomology and Insect Science"]},{"key":"thesis:degree_level","label":"Degree Level","values":["doctoral"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Arizona"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Anopheles stephensi","Lifespan and reproduction","Mosquito immunity","Mosquito insulin-like peptides","Mosquito metabolism","Transgenic mosquito"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction, presentation (such as public display or performance) of protected items is prohibited except with permission of the author."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10150/628409"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Malaria is a mosquito-borne disease caused by parasites belonging to the genus Plasmodium. Malaria remains one of the most devastating infectious diseases, killing nearly half a million people each year (WHO 2015). 1,2 With the current increase in drug and insecticide resistance, there is an urgent need to develop novel strategies for malaria control. One such strategy to genetically engineer mosquito vectors to make them resistant to infection by malaria parasites in order to replace the wild population with malaria refractory mosquitoes. The insulin/IGF-like signaling (IIS) pathway is one potential target for a population replacement strategy since it regulates metabolism, immunity, lifespan and reproduction in mosquitoes. We previously generated a transgenic Anopheles stephensi line with increased insulin signaling in the fat body. Surprisingly, these transgenic mosquitoes survived significantly longer than their non-transgenic siblings, while in nearly every other organism increased IIS resulted in a decrease in lifespan. In this work, we sought to define how the fat body IIS controls lifespan, and also to determine the impact of the fat body IIS on reproduction, metabolism, and Plasmodium resistance. We found that overexpression of the molecule Akt, a key IIS nexus molecule, resulted in an increased overall fitness and enhanced Plasmodium falciparum parasite resistance in transgenic Anopheles stephensi, as compared to their non-transgenic siblings. Overall results from these studies highlight the important role of IIS in the mosquito fat body in controlling lifespan, reproduction, metabolism and immunity."]},{"key":"dc:title","label":"Title","values":["Genetically Modifying Mosquitoes Without Compromising Fitness: Can It Be Done?"]}]}],"canonical_facts":{"dc:contributor.advisor":["Riehle, Michael A."],"dc:contributor.committeemember":["Walker, Kathleen R.","Miesfeld, Rorger L.","Jewett, John C."],"dc:creator":["Hun, Lewis Vibul"],"dc:date.accessioned":["2018-08-09T20:15:35Z"],"dc:date.available":["2018-08-09T20:15:35Z"],"dc:date.issued":["2018"],"dc:description.abstract":["Malaria is a mosquito-borne disease caused by parasites belonging to the genus Plasmodium. Malaria remains one of the most devastating infectious diseases, killing nearly half a million people each year (WHO 2015). 1,2 With the current increase in drug and insecticide resistance, there is an urgent need to develop novel strategies for malaria control. One such strategy to genetically engineer mosquito vectors to make them resistant to infection by malaria parasites in order to replace the wild population with malaria refractory mosquitoes. The insulin/IGF-like signaling (IIS) pathway is one potential target for a population replacement strategy since it regulates metabolism, immunity, lifespan and reproduction in mosquitoes. We previously generated a transgenic Anopheles stephensi line with increased insulin signaling in the fat body. Surprisingly, these transgenic mosquitoes survived significantly longer than their non-transgenic siblings, while in nearly every other organism increased IIS resulted in a decrease in lifespan. In this work, we sought to define how the fat body IIS controls lifespan, and also to determine the impact of the fat body IIS on reproduction, metabolism, and Plasmodium resistance. We found that overexpression of the molecule Akt, a key IIS nexus molecule, resulted in an increased overall fitness and enhanced Plasmodium falciparum parasite resistance in transgenic Anopheles stephensi, as compared to their non-transgenic siblings. Overall results from these studies highlight the important role of IIS in the mosquito fat body in controlling lifespan, reproduction, metabolism and immunity."],"dc:identifier.uri":["http://hdl.handle.net/10150/628409"],"dc:language.iso":["en"],"dc:publisher":["The University of Arizona."],"dc:rights":["Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction, presentation (such as public display or performance) of protected items is prohibited except with permission of the author."],"dc:subject":["Anopheles stephensi","Lifespan and reproduction","Mosquito immunity","Mosquito insulin-like peptides","Mosquito metabolism","Transgenic mosquito"],"dc:title":["Genetically Modifying Mosquitoes Without Compromising Fitness: Can It Be Done?"],"dc:type":["text","Electronic Dissertation"],"thesis:degree_discipline":["Graduate College","Entomology and Insect Science"],"thesis:degree_level":["doctoral"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Arizona"]},"updated_at":"2026-07-24T00:55:10Z"}