Juvenile hormone and its receptor methoprene-tolerant promote ribosomal biogenesis and vitellogenesis in the Aedes aegypti mosquito
- From the ‡Department of Entomology, University of California, Riverside, California 92521,
- §Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan 430079, China,
- ¶Institute for Integrative Genomic Biology, University of California, Riverside, California 92521,
- ‖Key Laboratory of Tropical Marine Bio-Resources and Ecology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou 510301, China, and
- **Guizhou Key Laboratory for Plant Pest Management of Mountain Region, College of Agriculture, Guizhou University, Guiyang 550025, China
- ↵1 To whom correspondence should be addressed. E-mail: alexander.raikhel{at}ucr.edu.
-
Edited by Ronald C. Wek
Abstract
Juvenile hormone (JH) controls many biological activities in insects, including development, metamorphosis, and reproduction. In the Aedes aegypti mosquito, a vector of dengue, yellow fever, chikungunya, and zika viruses, the metabolic tissue (the fat body, which is an analogue of the vertebrate liver) produces yolk proteins for developing oocytes. JH is important for the fat body to acquire competence for yolk protein production. However, the molecular mechanisms of how JH promotes mosquito reproduction are not completely understood. In this study we show that stimulation of the JH receptor methoprene-tolerant (Met) activates expression of genes encoding the regulator of ribosome synthesis 1 (RRS1) and six ribosomal proteins (two ribosomal large subunit proteins, two ribosomal small subunit proteins, and two mitochondrial ribosomal proteins). Moreover, RNAi-mediated depletion of RRS1 decreased biosynthesis of the ribosomal protein L32 (RpL32). Depletion of Met, RRS1, or RpL32 led to retardation of ovarian growth and reduced mosquito fecundity, which may at least in part have resulted from decreased vitellogenin protein production in the fat body. In summary, our results indicate that JH is critical for inducing the expression of ribosomal protein genes and demonstrate that RRS1 mediates the JH signal to enhance both ribosomal biogenesis and vitellogenesis.
Footnotes
-
This work was supported by National Institutes of Health Grant R01 AI036959 (to A. S. R.). This work was also supported by Scholar Fellowship 201506775010 (to J.-L. W.) from the China Scholarship Council of Chinese Ministry of Education. The authors declare that they have no conflicts of interest regarding the content of this article. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
-
This article contains supplemental Tables S1 and S2.
- Received September 30, 2016.
- Revision received April 24, 2017.
- © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.
