2015
DOI: 10.1016/j.gene.2015.06.032
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Characterization of two juvenile hormone epoxide hydrolases by RNA interference in the Colorado potato beetle

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Cited by 32 publications
(25 citation statements)
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“…Instead, JHEH is a member of the microsomal epoxide hydrolases, which are non-secreted enzymes, active in different organs and tissues. JHEH is responsible for irreversibly opening the epoxide ring of JH to produce JH diol 10,11 . Finally, JHDK catalyzes the phosphorylation of JH diol to produce a more water-soluble metabolite 12,13 .…”
Section: Introductionmentioning
confidence: 99%
“…Instead, JHEH is a member of the microsomal epoxide hydrolases, which are non-secreted enzymes, active in different organs and tissues. JHEH is responsible for irreversibly opening the epoxide ring of JH to produce JH diol 10,11 . Finally, JHDK catalyzes the phosphorylation of JH diol to produce a more water-soluble metabolite 12,13 .…”
Section: Introductionmentioning
confidence: 99%
“…JHEHs are crucial enzymes responsible for JH degradation, and are potential targets for selective insecticidal compounds. The cD-NAs of JHEH genes from several insect species have been cloned, including Trichoplusia ni Hübner (Lepidoptera: Noctuidae) (Harris et al 1999), Ctenocephalides felis (Bouche) (Siphonaptera: Pulicidae) (Keiser et al 2002), Bombyx mori L. (Lepidoptera: Bombycidae) (Zhang et al 2005), Apis mellifera L. (Hymenoptera: Apidae) (Mackert et al 2010), Tribolium castaneum (Herbst) (Coleoptera: Tenebrionidae) (Tsubota et al 2010b), Homalodisca vitripennis (Germar) (Hemiptera: Cicadellidae) (Kamita et al 2013), Manduca sexta L. (Lepidopetra: Sphingidae) (Wojtasek & Prestwich 1996), and Leptinotarsa decemlineata (Say) (Coleoptera: Chrysomelidae) (Lü et al 2015). The ability of recombinant JHEHs to degrade JH in vitro has been confirmed in several insect species (Keiser et al 2002;Zhang et al 2005;Tsubota et al 2010b;Kamita et al 2013).…”
mentioning
confidence: 99%
“…At the wandering stage, JH titer obviously decreased [41], and the expression of JH degradation genes were activated [39]. Here we found that ingestion of JH (Fig 2F), or knockdown of an allatostatin gene ( AS-C ) [41] or either of two JH degradation genes (JH epoxide hydrolase, JHEH1 ; JH diol kinase, JHDK ) [35, 39] to delay JH decrease significantly reduced light avoidance (Fig 2G and S1E-G Fig) and postponed the occurrence of wandering (S2 Table); whereas knockdown of a JH biosynthesis gene (JH acid methyl transferase, JHAMT ) [34] and a JH receptor gene (methoprene-tolerant, Met ) to prematurely reduce JH signal enhanced light avoidance (Fig 2H and S1H, I Fig) and accelerated the onset of wandering (S2 Table). It is clear that JH signal inhibits the premature switch of light preference and the early onset of wandering.…”
Section: Resultsmentioning
confidence: 99%