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

Nov 1, 2015The Journal of biological chemistry

Krüppel Homolog 1 may block insect metamorphosis by directly turning off a gene that controls pupal development

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Abstract

Krüppel homolog 1 (Kr-h1) protein directly binds to the Kr-h1 binding site in the Broad-Complex gene (BR-C) promoter and represses its activation.

The expression of BR-C is induced by molting hormone (20-hydroxyecdysone) and repressed by juvenile hormone (JH).
Kr-h1 is induced by JH and is responsible for repressing the expression of BR-C.
Forced expression of Kr-h1 inhibits the activation of the BR-C promoter by 20E in the absence of JH.
Kr-h1 RNA interference disrupts JH-mediated repression of BR-C.
Deletion of the Kr-h1 binding site from the BR-C promoter abolishes its repression.
Two Kr-h1 molecules bind to the Kr-h1 binding site in the BR-C promoter.

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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 RNAi 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.

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

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