Abstract
Juvenile hormone (JH) is important for multiple aspects of insect development and physiology. Although roles of JH have received considerable studies, JH signaling pathway at the molecular level is still not well understood. Methoprenetolerant (Met) in Drosophila melanogaster fulfills many of the requirements as a hormone receptor gene. A paralogous gene, germ-cell expressed (gce), possesses homology to Met and is a candidate as a Met partner in mediating JH action. To probe roles of this gene in JH action, we carried out in vivo gce underexpression studies using RNAi technique. Precocious expression of broad (br) gene was found to occur when gce was knocked down in the young larvae. We also demonstrated that RNA interference-driven knockdown of gce expression in transgenic flies results in appearance of resistance to pyriproxyfen (IGRs). These results show that gce is a vital gene and appears to promote JH action in larval stages.
Highlights
Drosophila melanogaster (Order: Diptera; Family: Drosophilidae) provides an ideal system to examine the genes and molecular mechanisms of hormones that regulate the growth and differentiation of tissue
When a long double stranded RNA (dsRNA) is introduced into the organism, its double-stranded structure is recognized by a ribonuclease III enzyme named Dicer, which subsequently cleaves it into smaller fragments named small interfering RNAs
More recent works based on RNA interference (RNAi) experiments have shown that the transcription factor Broad and Kruppel homolog 1 are involved in the antimetamorphic action of Juvenile hormone (JH) (Minakuchi et al, 2009)
Summary
Drosophila melanogaster (Order: Diptera; Family: Drosophilidae) provides an ideal system to examine the genes and molecular mechanisms of hormones that regulate the growth and differentiation of tissue. Researchers developed a large scale RNAi injection method for Drosophila embryos to identify and characterize the molecular functions of the 14,000 Drosophila genes (Cornell et al 2008). RNAi can be triggered by the expression of a long double stranded hairpin RNA from a transgene containing a gene fragment cloned as an inverted repeat. The expression of such transgenes under the control of a generic promoter containing the Gal4-responsive upstream activator sequence (UAS) element can target RNAi to any cell type at any stage of the insect for which a suitable Gal driver line is available (Bellés 2010)
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