Krüppel homolog 1, an early juvenile hormone-response gene downstream of Methoprene-tolerant, mediates its anti-metamorphic action in the red flour beetle Tribolium castaneum

Minakuchi, Chieka; Namiki, Toshiki; Shinoda, Tetsuro

doi:10.1016/j.ydbio.2008.10.016

Cited by 291 publications

(340 citation statements)

References 39 publications

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“…1B). These results clearly showed that the expression of BmKr-h1 was positively regulated by JH in B. mori larvae, as has been reported in other insect species (19,20,22,23).…”

Section: Resultssupporting

confidence: 87%

“…We reported that the Kr-h1 homolog in T. castaneum (TcKr-h1) also is induced rapidly by JH, and knockdown of TcKrh1 causes precocious metamorphosis (20), as is seen in the knockdown of TcMet (10, 11). Moreover, an RNAi silencing analysis showed that TcKr-h1 works downstream of TcMet (20). Taken together, the available information indicates that Kr-h1 may play a primary role in the repression of metamorphosis in close cooperation with Met.…”

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confidence: 99%

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Transcriptional regulation of juvenile hormone-mediated induction of Krüppel homolog 1, a repressor of insect metamorphosis

Kayukawa

Minakuchi²,

Namiki³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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The Krüppel homolog 1 gene (Kr-h1) has been proposed to play a key role in the repression of insect metamorphosis. Kr-h1 is assumed to be induced by juvenile hormone (JH) via a JH receptor, methoprene-tolerant (Met), but the mechanism of induction is unclear. To elucidate the molecular mechanism of Kr-h1 induction, we first cloned cDNAs encoding Kr-h1 (BmKr-h1) and Met (BmMet1 and BmMet2) homologs from Bombyx mori. In a B. mori cell line, BmKrh1 was rapidly induced by subnanomolar levels of natural JHs. Reporter assays identified a JH response element (kJHRE), comprising 141 nucleotides, located ∼2 kb upstream from the BmKr-h1 transcription start site. The core region of kJHRE (GGCCTCCACGTG) contains a canonical E-box sequence to which Met, a basic helix-loophelix Per-ARNT-Sim (bHLH-PAS) transcription factor, is likely to bind. In mammalian HEK293 cells, which lack an intrinsic JH receptor, ectopic expression of BmMet2 fused with Gal4DBD induced JHdependent activity of an upstream activation sequence reporter. Meanwhile, the kJHRE reporter was activated JH-dependently in HEK293 cells only when cotransfected with BmMet2 and BmSRC, another bHLH-PAS family member, suggesting that BmMet2 and BmSRC jointly interact with kJHRE. We also found that the interaction between BmMet2 and BmSRC is dependent on JH. Therefore, we propose the following hypothesis for the mechanism of JHmediated induction of BmKr-h1: BmMet2 accepts JH as a ligand, JH-liganded BmMet2 interacts with BmSRC, and the JH/BmMet2/ BmSRC complex activates BmKr-h1 by interacting with kJHRE. development | insecticide | steroid receptor coactivator

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“…1B). These results clearly showed that the expression of BmKr-h1 was positively regulated by JH in B. mori larvae, as has been reported in other insect species (19,20,22,23).…”

Section: Resultssupporting

confidence: 87%

mentioning

confidence: 99%

Transcriptional regulation of juvenile hormone-mediated induction of Krüppel homolog 1, a repressor of insect metamorphosis

Kayukawa

Minakuchi²,

Namiki³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…Kr-h1 proteins commonly have eight C 2 H 2 zinc finger domains, which putatively bind to a specific DNA sequence (9,17). We hypothesized that BmKr-h1 directly binds to the BmBR-C_P dist region and represses the activation of BmBR-C_P dist by 20E.…”

Section: Identification Of Kbs In the Br-c Promoter-insectmentioning

confidence: 99%

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

Kayukawa

Nagamine

Ito

et al. 2016

Journal of Biological Chemistry

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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.The molting and metamorphosis of insects are intricately regulated by the actions and interactions of ecdysteroids and juvenile hormone (JH).2 In holometabolous insects, 20-hydroxyecdysone (20E, the primary active ecdysteroid) induces the larval-larval molt in the presence of JH. When the JH titer declines to a trace level in the final larval instar, 20E induces larval-pupal and pupal-adult molts (metamorphosis). Thus, JH plays a key role in preventing larvae from undergoing precocious metamorphosis (1).Our understanding of the molecular mechanism of JH-mediated repression of insect metamorphosis has significantly advanced (2): JH carried to a target cell is received by a JH receptor, methoprene tolerant (Met) (3-6); JH-liganded Met interacts with steroid receptor coactivator (7-12); the JH/Met/ steroid receptor coactivator complex activates Krüppel homolog 1 (Kr-h1), a repressor of metamorphosis, by interacting with a JH response element (kJHRE) in the Kr-h1 gene (9, 10, 12-15); Kr-h1 represses the larval-pupal metamorphosis (16 -20). To date, however, the mechanism of the repression of metamorphosis by Kr-h1, including target gene(s), binding site(s), and partner(s), has remained unknown.The Broad-Complex (BR-C) protein is a transcription factor that is composed of a Bric-a-brac/Tramtrack/Broad-Complex (BTB) domain and an alternatively spliced zinc finger domain (Z1-Z6) (21-25). BR-C expression is induced by 20E, ...

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“…The Drosophila Krüppel homolog 1 (Kr-h1) gene encodes a zinc-finger motif transcription factor, which has been implicated in larval-pupal metamorphosis (16). It is now used as a representative marker gene under the regulation of JH and MET (14,(17)(18)(19). The Hairy gene encodes a bHLH protein with an orange domain and C-terminal Groucho interacting motifs (20).…”

Section: Cyc Is a Jh Iii-dependent Met-interacting Protein In A Aegmentioning

confidence: 99%

bHLH-PAS heterodimer of methoprene-tolerant and Cycle mediates circadian expression of juvenile hormone-induced mosquito genes

Shin

Zou

Saha

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

116

108

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Juvenile hormone (JH) governs a great diversity of processes in insect development and reproduction. It plays a critical role in controlling the gonadotrophic cycles of female mosquitoes by preparing tissues for blood digestion and egg development. Here, we show that in female Aedes aegypti mosquitoes JH III control of gene expression is mediated by a heterodimer of two bHLH-PAS proteins-the JH receptor methoprene-tolerant (MET) and Cycle (CYC, AAEL002049). We identified Aedes CYC as a MET-interacting protein using yeast two-hybrid screening. Binding of CYC and MET required the presence of JH III. In newly eclosed female mosquitoes, the expression of two JH-responsive genes, Kr-h1 and Hairy, was dependent on both the ratio of light to dark periods and JH III. Their expression was compromised by in vivo RNA interference (RNAi) depletions of CYC, MET, and the steroid receptor coactivator SRC/FISC. Moreover, JH III was not effective in induction of Krh1 and Hairy gene expression in vitro in fat bodies of female mosquitoes with RNAi-depleted CYC, MET or SRC/FISC. A sequence containing an E-box-like motif from the Aedes Kr-h1 gene promoter specifically interacted with a protein complex, which included MET and CYC from the female mosquito fat body nuclear extract. These results indicate that a MET/CYC heterodimer mediates JH III activation of Kr-h1 and Hairy genes in the context of light-dependent circadian regulation in female mosquitoes during posteclosion development. This study provides an important insight into the understanding of the molecular basis of JH action.hormone receptor | insect hormone | transcriptional control M osquitoes serve as vectors of harmful human diseases because blood feeding is required for their egg development; disease pathogens use hematophagous female mosquitoes for obligatory stages of their life cycles. An insect-specific sesquiterpenoid juvenile hormone III (JH III) is essential for a newly eclosed female mosquito to reach a competence stage for blood feeding and egg maturation (1, 2). Although several aspects of the JH III-dependent development have been characterized (3-6), our understanding of molecular mechanisms underlying JH regulation of female mosquito posteclosion development is limited.Methoprene-tolerant (MET), which is a basic helix-loop-helix (bHLH)-Per-Arnt-Sim (PAS) protein, was discovered in Drosophila melanogaster (7), and its role in mediating a JH response has been established (8). MET binds to JH with a high affinity, suggesting that it is the JH receptor (9, 10). As a bHLH protein, MET requires either a homo-or heterodimer partner for its activity (11). Studies in Aedes aegypti, the beetle Tribolium castaneum, and the silkworm Bombyx mori have shown a bHLH-PAS domain-containing steroid receptor coactivator (SRC/FISC/ Taiman) to interact with MET (10,[12][13][14]. Whether, an additional bHLH transcription factor with DNA-binding properties is required as a Met partner remains to be established.Using yeast two-hybrid (Y2H) screening, we identified an Aedes ortholo...

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Krüppel homolog 1, an early juvenile hormone-response gene downstream of Methoprene-tolerant, mediates its anti-metamorphic action in the red flour beetle Tribolium castaneum

Cited by 291 publications

References 39 publications

Transcriptional regulation of juvenile hormone-mediated induction of Krüppel homolog 1, a repressor of insect metamorphosis

Transcriptional regulation of juvenile hormone-mediated induction of Krüppel homolog 1, a repressor of insect metamorphosis

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

bHLH-PAS heterodimer of methoprene-tolerant and Cycle mediates circadian expression of juvenile hormone-induced mosquito genes

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