{"id":{"repo_id":"wfu","oai_identifier":"oai:wakespace.lib.wfu.edu:10339/62638"},"canonical_url":"https://search.dev.ndltd.org/etd/wfu/oai:wakespace.lib.wfu.edu:10339/62638","repository":{"repo_id":"wfu","name":"Wake Forest University","base_url":"https://wakespace.lib.wfu.edu/oai/request"},"display":{"title":"Evaluation of Adipokinetic Hormone Receptor Function Suggests a Single Tissue is Responsible for Starvation Phenotypes in Drosophila.","abstract":"Adipokinetic hormone (AKH) is an insect neurohormone critical in times of metabolic stress. AKH signals to the fat body where it induces both hypertrehalosemia and hyperlipemia. AKH secretion also leads to starvation-induced hyperactivity, a foraging behavior. Genetic ablation of AKH cells or a genetic deletion of the AKH receptor (AKHR) results in flies that lack starvation-induced hyperactivity and have decreased lipid and trehalose hemolymph levels, and are, consequently, long-lived under starvation conditions. This study aimed to determine the anatomical basis of AKHR signaling for starvation phenotypes. Genetic knockdown of the AKHR via a specific RNAi element in multiple driver lines increased starvation longevity similar to that seen with an AKHR null mutant. These GAL4s define phenotypically relevant sites of AKHR expression, and a systematic evaluation of the tissues captured by these driver lines detected that several directed expression in the fat body. Genetic rescue of AKHR function in fat body restored wild type starvation longevity and locomotion, indicating receptor expression in the fat body is sufficient for these phenotypes. The AKHR can couple to either Gαs or Gαq in heterologous expression systems, but this study is the first example of quantification of AKHR signaling in vivo. Injection of AKH into intact animals causes calcium levels within the fat body to rise, and this response is absent in flies with a fat body specific knockdown of AKHR, demonstrating that calcium increases in the fat body depend upon the AKH receptor. This study suggests that a single tissue, the fat body, is responsible for AKH-dependent starvation phenotypes in Drosophila, and indicates that AKH causes an AKHR-dependent increase in calcium in this tissue.","abstract_html":"Adipokinetic hormone (AKH) is an insect neurohormone critical in times of metabolic stress. AKH signals to the fat body where it induces both hypertrehalosemia and hyperlipemia. AKH secretion also leads to starvation-induced hyperactivity, a foraging behavior. Genetic ablation of AKH cells or a genetic deletion of the AKH receptor (AKHR) results in flies that lack starvation-induced hyperactivity and have decreased lipid and trehalose hemolymph levels, and are, consequently, long-lived under starvation conditions. This study aimed to determine the anatomical basis of AKHR signaling for starvation phenotypes. Genetic knockdown of the AKHR via a specific RNAi element in multiple driver lines increased starvation longevity similar to that seen with an AKHR null mutant. These GAL4s define phenotypically relevant sites of AKHR expression, and a systematic evaluation of the tissues captured by these driver lines detected that several directed expression in the fat body. Genetic rescue of AKHR function in fat body restored wild type starvation longevity and locomotion, indicating receptor expression in the fat body is sufficient for these phenotypes. The AKHR can couple to either Gαs or Gαq in heterologous expression systems, but this study is the first example of quantification of AKHR signaling in vivo. Injection of AKH into intact animals causes calcium levels within the fat body to rise, and this response is absent in flies with a fat body specific knockdown of AKHR, demonstrating that calcium increases in the fat body depend upon the AKH receptor. This study suggests that a single tissue, the fat body, is responsible for AKH-dependent starvation phenotypes in Drosophila, and indicates that AKH causes an AKHR-dependent increase in calcium in this tissue.","abstract_has_math":false,"creators":["Perry, Rebecca Jane"],"institution":"Wake Forest University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2016,"date_issued":"2016","date_published":"2016","updated_at":"2026-07-27T22:02:05Z","subjects":["adipokinetic hormone receptor"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10339/62638","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Perry, Rebecca Jane"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2016-08-25T08:35:21Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2018-08-19T08:30:10Z"]},{"key":"dc:date.issued","label":"Date","values":["2016"]},{"key":"dc:publisher","label":"Institution","values":["Wake Forest University"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["adipokinetic hormone receptor"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10339/62638"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Adipokinetic hormone (AKH) is an insect neurohormone critical in times of metabolic stress. AKH signals to the fat body where it induces both hypertrehalosemia and hyperlipemia. AKH secretion also leads to starvation-induced hyperactivity, a foraging behavior. Genetic ablation of AKH cells or a genetic deletion of the AKH receptor (AKHR) results in flies that lack starvation-induced hyperactivity and have decreased lipid and trehalose hemolymph levels, and are, consequently, long-lived under starvation conditions. This study aimed to determine the anatomical basis of AKHR signaling for starvation phenotypes. Genetic knockdown of the AKHR via a specific RNAi element in multiple driver lines increased starvation longevity similar to that seen with an AKHR null mutant. These GAL4s define phenotypically relevant sites of AKHR expression, and a systematic evaluation of the tissues captured by these driver lines detected that several directed expression in the fat body. Genetic rescue of AKHR function in fat body restored wild type starvation longevity and locomotion, indicating receptor expression in the fat body is sufficient for these phenotypes. The AKHR can couple to either Gαs or Gαq in heterologous expression systems, but this study is the first example of quantification of AKHR signaling in vivo. Injection of AKH into intact animals causes calcium levels within the fat body to rise, and this response is absent in flies with a fat body specific knockdown of AKHR, demonstrating that calcium increases in the fat body depend upon the AKH receptor. This study suggests that a single tissue, the fat body, is responsible for AKH-dependent starvation phenotypes in Drosophila, and indicates that AKH causes an AKHR-dependent increase in calcium in this tissue."]},{"key":"dc:title","label":"Title","values":["Evaluation of Adipokinetic Hormone Receptor Function Suggests a Single Tissue is Responsible for Starvation Phenotypes in Drosophila."]}]}],"canonical_facts":{"dc:creator":["Perry, Rebecca Jane"],"dc:date.accessioned":["2016-08-25T08:35:21Z"],"dc:date.available":["2018-08-19T08:30:10Z"],"dc:date.issued":["2016"],"dc:description.abstract":["Adipokinetic hormone (AKH) is an insect neurohormone critical in times of metabolic stress. AKH signals to the fat body where it induces both hypertrehalosemia and hyperlipemia. AKH secretion also leads to starvation-induced hyperactivity, a foraging behavior. Genetic ablation of AKH cells or a genetic deletion of the AKH receptor (AKHR) results in flies that lack starvation-induced hyperactivity and have decreased lipid and trehalose hemolymph levels, and are, consequently, long-lived under starvation conditions. This study aimed to determine the anatomical basis of AKHR signaling for starvation phenotypes. Genetic knockdown of the AKHR via a specific RNAi element in multiple driver lines increased starvation longevity similar to that seen with an AKHR null mutant. These GAL4s define phenotypically relevant sites of AKHR expression, and a systematic evaluation of the tissues captured by these driver lines detected that several directed expression in the fat body. Genetic rescue of AKHR function in fat body restored wild type starvation longevity and locomotion, indicating receptor expression in the fat body is sufficient for these phenotypes. The AKHR can couple to either Gαs or Gαq in heterologous expression systems, but this study is the first example of quantification of AKHR signaling in vivo. Injection of AKH into intact animals causes calcium levels within the fat body to rise, and this response is absent in flies with a fat body specific knockdown of AKHR, demonstrating that calcium increases in the fat body depend upon the AKH receptor. This study suggests that a single tissue, the fat body, is responsible for AKH-dependent starvation phenotypes in Drosophila, and indicates that AKH causes an AKHR-dependent increase in calcium in this tissue."],"dc:identifier.uri":["http://hdl.handle.net/10339/62638"],"dc:language.iso":["en"],"dc:publisher":["Wake Forest University"],"dc:subject":["adipokinetic hormone receptor"],"dc:title":["Evaluation of Adipokinetic Hormone Receptor Function Suggests a Single Tissue is Responsible for Starvation Phenotypes in Drosophila."],"dc:type":["Thesis"]},"updated_at":"2026-07-27T22:02:05Z"}