作者: T. Kayukawa , C. Minakuchi , T. Namiki , T. Togawa , M. Yoshiyama
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摘要: The Kruppel homolog 1 gene (Kr-h1) has been proposed to play a key role in the repression of insect metamorphosis. Kr-h1 is assumed be induced by juvenile hormone (JH) via JH receptor, methoprene-tolerant (Met), but mechanism induction unclear. To elucidate molecular induction, we first cloned cDNAs encoding (BmKr-h1) and Met (BmMet1 BmMet2) homologs from Bombyx mori. In B. mori cell line, BmKr-h1 was rapidly subnanomolar levels natural JHs. Reporter assays identified response element (kJHRE), comprising 141 nucleotides, located ∼2 kb upstream transcription start site. core region kJHRE (GGCCTCCACGTG) contains canonical E-box sequence which Met, basic helix–loop–helix Per-ARNT-Sim (bHLH–PAS) factor, likely bind. mammalian HEK293 cells, lack an intrinsic ectopic expression BmMet2 fused with Gal4DBD JH-dependent activity activation reporter. Meanwhile, reporter activated JH-dependently cells only when cotransfected BmSRC, another bHLH–PAS family member, suggesting that BmSRC jointly interact kJHRE. We also found interaction between dependent on JH. Therefore, propose following hypothesis for JH-mediated BmKr-h1: accepts as ligand, JH-liganded interacts JH/BmMet2/BmSRC complex activates interacting