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Ecdysone receptor isoform‐B mediates soluble trehalase expression to regulate growth and development in the mirid bug, A polygus lucorum ( M eyer‐ D ür)
Author(s) -
Tan Y.A.,
Xiao L.B.,
Zhao J.,
Xiao Y.F.,
Sun Y.,
Bai L.X.
Publication year - 2015
Publication title -
insect molecular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.955
H-Index - 93
eISSN - 1365-2583
pISSN - 0962-1075
DOI - 10.1111/imb.12185
Subject(s) - trehalase , biology , gene knockdown , ecdysone receptor , trehalose , gene isoform , gene expression , rna interference , messenger rna , midgut , receptor , microbiology and biotechnology , biochemistry , gene , rna , transcription factor , botany , nuclear receptor , larva
Ecdysone receptor ( EcR ) is the hormonal receptor of ecdysteroids and strictly regulates growth and development in insects. However, the action mechanism of EcR is not very clear. In this study, the cDNA of EcR isoform‐B was cloned from Apolygus lucorum ( AlEcR ‐B) and its expression profile was investigated. We reduced AlEcR‐B mRNA expression using systemic RNA interference in vivo , and obtained knockdown specimens. Examination of these specimens indicated that AlEcR‐B is required for nymphal survival, and that reduced expression is associated with longer development time and lower nymphal weight. To investigate the underlying molecular mechanism of the observed suppression effects, we selected trehalase for a detailed study. Transcript encoding soluble trehalase ( AlTre‐1 ) was up‐regulated by 20‐hydroxyecdysone and in agreement with the mRNA expression of AlEcR‐B . The expression profile of AlTre‐1 , soluble trehalase activity and translated protein level in the midgut of surviving nymphs were down‐regulated, compared with controls, after the knockdown expression of AlEcR‐B . By contrast, membrane‐bound trehalase activity, the related gene expression and translated protein level remained at their initial levels. However, trehalose content significantly increased and the glucose content significantly decreased under the same conditions. We propose that AlEcR‐B controls normal carbohydrate metabolism by mediating the expression of AlTre‐1 to regulate the growth and development in A. lucorum , which provide an extended information into the functions of AlEcR‐B .