title: Hormone and receptor interplay in the regulation of mosquito lipid metabolism.
abstract: Mosquitoes transmit devastating human diseases because they need vertebrate blood for egg development. Metabolism in female mosquitoes is tightly coupled with blood meal-mediated reproduction, which requires an extremely high level of energy consumption. Functional analysis has shown that major genes encoding for enzymes involved in lipid metabolism (LM) in the mosquito fat bodies are down-regulated at the end of the juvenile hormone (JH)-controlled posteclosion (PE) phase but exhibit significant elevation in their transcript levels during the post-blood meal phase (PBM), which is regulated mainly by 20-hydroxyecdysone (20E). Reductions in the transcript levels of genes encoding triacylglycerol (TAG) catabolism and β-oxidation enzymes were observed to correlate with a dramatic accumulation of lipids in the PE phase; in contrast, these transcripts were elevated significantly and lipid stores were diminished during the PBM phase. The RNAi depletion of Methoprene-tolerant (Met) and ecdysone receptor (EcR), receptors for JH and 20E, respectively, reversed the LM gene expression and the levels of lipid stores and metabolites, demonstrating the critical roles of these hormones in LM regulation. Hepatocyte nuclear factor 4 (HNF4) RNAi-silenced mosquitoes exhibited down-regulation of the gene transcripts encoding TAG catabolism and β-oxidation enzymes and an inability to use lipids effectively, as manifested by TAG accumulation. The luciferase reporter assay showed direct regulation of LM-related genes by HNF4. Moreover,HNF4gene expression was down-regulated by Met and activated by EcR and Target of rapamycin, providing a link between nutritional and hormonal regulation of LM in female mosquitoes.
authors.affiliation: State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, People's Republic of China.|University of Chinese Academy of Sciences, Beijing 100049, People's Republic of China.
authors.forename: Xueli
authors.initials: X
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, People's Republic of China.|University of Chinese Academy of Sciences, Beijing 100049, People's Republic of China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Hou
authors.affiliation: Department of Entomology, University of California, Riverside, CA 92521.
authors.forename: Tusar T
authors.initials: TT
authors.lastname: Saha
authors.affiliation: State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, People's Republic of China.|University of Chinese Academy of Sciences, Beijing 100049, People's Republic of China.
authors.forename: Gaofeng
authors.initials: G
authors.lastname: Pei
authors.affiliation: Department of Entomology, University of California, Riverside, CA 92521; alexander.raikhel@ucr.edu zouzhen@ioz.ac.cn.|Institute for Integrative Genome Biology, University of California, Riverside, CA 92521.
authors.forename: Alexander S
authors.initials: AS
authors.lastname: Raikhel
authors.affiliation: State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, People's Republic of China; alexander.raikhel@ucr.edu zouzhen@ioz.ac.cn.|University of Chinese Academy of Sciences, Beijing 100049, People's Republic of China.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Zou
mesh_terms: D000330:Aedes / Q000378:metabolism*; D000818:Animals; D005260:Female; D007301:Insect Hormones / Q000378:metabolism / Q000502:physiology*; D007305:Insecticide Resistance / Q000235:genetics; D050356:Lipid Metabolism; D053858:Metabolic Networks and Pathways; D012098:Reproduction
chemical_list: D007301:Insect Hormones
keywords: 20-hydroxyecdysone; beta-oxidation; hepatocyte nuclear factor 4; juvenile hormone; lipid