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Krüppel Homolog 1 Inhibits Insect Metamorphosis via Direct Transcriptional Repression of Broad-Complex, a Pupal Specifier Gene.

J Biol Chem. 2016 Jan 22;291(4):1751-62. Epub 2015 Oct 30
Takumi Kayukawa 1 , Keisuke Nagamine 2 , Yuka Ito 3 , Yoshinori Nishita 4 , Yukio Ishikawa 5 , Tetsuro Shinoda 3
Takumi Kayukawa 1 , Keisuke Nagamine 2 , Yuka Ito 3 , Yoshinori Nishita 4 , Yukio Ishikawa 5 , Tetsuro Shinoda 3
+ et al

[No authors listed]

Author information
  • 1 From the Insect Growth Regulation Research Unit, National Institute of Agrobiological Sciences, Tsukuba, Ibaraki 305-8634, Japan, kayu@affrc.go.jp.
  • 2 From the Insect Growth Regulation Research Unit, National Institute of Agrobiological Sciences, Tsukuba, Ibaraki 305-8634, Japan, Laboratory of Applied Entomology, Graduate School of Agricultural and Life Sciences, University of Tokyo, Bunkyo, Tokyo 113-8657, Japan, and.
  • 3 From the Insect Growth Regulation Research Unit, National Institute of Agrobiological Sciences, Tsukuba, Ibaraki 305-8634, Japan.
  • 4 Department of Biological Science and Center for Genome Dynamics, Faculty of Science, Hokkaido University, Sapporo, Hokkaido 060-0810, Japan.
  • 5 Laboratory of Applied Entomology, Graduate School of Agricultural and Life Sciences, University of Tokyo, Bunkyo, Tokyo 113-8657, Japan, and.

摘要


The Broad-Complex gene (BR-C) encodes transcription factors that dictate larval-pupal metamorphosis in insects. The expression of BR-C is induced by molting hormone (20-hydroxyecdysone (20E)), and this induction is repressed by juvenile hormone (JH), which exists during the premature larval stage. Krüppel homolog 1 gene (Kr-h1) has been known as a JH-early inducible gene responsible for repression of metamorphosis; however, the functional relationship between Kr-h1 and repression of BR-C has remained unclear. To elucidate this relationship, we analyzed cis- and trans elements involved in the repression of BR-C using a Bombyx mori cell line. In the cells, as observed in larvae, JH induced the expression of Kr-h1 and concurrently suppressed 20E-induced expression of BR-C. Forced expression of Kr-h1 repressed the 20E-dependent activation of the BR-C promoter in the absence of JH, and Kr-h1 inhibited the JH-mediated repression, suggesting that Kr-h1 controlled the repression of BR-C. A survey of the upstream sequence of BR-C gene revealed a Kr-h1 binding site (KBS) in the BR-C promoter. When KBS was deleted from the promoter, the repression of BR-C was abolished. Electrophoresis mobility shift demonstrated that two Kr-h1 molecules bound to KBS in the BR-C promoter. Based on these results, we conclude that Kr-h1 protein molecules directly bind to the KBS sequence in the BR-C promoter and thereby repress 20E-dependent activation of the pupal specifier, BR-C. This study has revealed a considerable portion of the picture of JH signaling pathways from the reception of JH to the repression of metamorphosis.

KEYWORDS: development, endocrinology, hormone, insect, signaling