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First published online May 22, 2009
doi: 10.1242/10.1242/dev.033712

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Juvenile hormone counteracts the bHLH-PAS transcription factors MET and GCE to prevent caspase-dependent programmed cell death in Drosophila

Ying Liu^1,*, Zhentao Sheng^1,*, Hanhan Liu¹, Di Wen¹, Qianyu He¹, Sheng Wang¹, Wei Shao¹, Rong-Jing Jiang¹, Shiheng An², Yaning Sun², William G. Bendena³, Jian Wang⁴, Lawrence I. Gilbert⁵, Thomas G. Wilson⁶, Qisheng Song^2, and Sheng Li^1,

¹ Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China.
² Division of Plant Sciences, University of Missouri, Columbia, MO 65211, USA.
³ Department of Biology, Queen's University, Kingston, Ontario K7L 3N6, Canada.
⁴ Department of Entomology, University of Maryland, College Park, MD 20742, USA.
⁵ Department of Biology, University of North Carolina, Chapel Hill, NC 27599, USA.
⁶ Department of Entomology, Ohio State University, Columbus, OH 43210, USA.

Authors for correspondence: (e-mails: songQ{at}missouri.edu; shengli{at}sippe.ac.cn)

Accepted 16 April 2009

Juvenile hormone (JH) regulates many developmental and physiological events in insects, but its molecular mechanism remains conjectural. Here we report that genetic ablation of the corpus allatum cells of the Drosophila ring gland (the JH source) resulted in JH deficiency, pupal lethality and precocious and enhanced programmed cell death (PCD) of the larval fat body. In the fat body of the JH-deficient animals, Dronc and Drice, two caspase genes that are crucial for PCD induced by the molting hormone 20-hydroxyecdysone (20E), were significantly upregulated. These results demonstrated that JH antagonizes 20E-induced PCD by restricting the mRNA levels of Dronc and Drice. The antagonizing effect of JH on 20E-induced PCD in the fat body was further confirmed in the JH-deficient animals by 20E treatment and RNA interference of the 20E receptor EcR. Moreover, MET and GCE, the bHLH-PAS transcription factors involved in JH action, were shown to induce PCD by upregulating Dronc and Drice. In the Met- and gce-deficient animals, Dronc and Drice were downregulated, whereas in the Met-overexpression fat body, Dronc and Drice were significantly upregulated leading to precocious and enhanced PCD, and this upregulation could be suppressed by application of the JH agonist methoprene. For the first time, we demonstrate that JH counteracts MET and GCE to prevent caspase-dependent PCD in controlling fat body remodeling and larval-pupal metamorphosis in Drosophila.

Key words: Juvenile hormone, 20-hydroxyecdysone, Dronc (Nc), Drice (Ice), Met, gce, Fat body, Metamorphosis, Programmed cell death, Drosophila melanogaster

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