title: Wnt signaling cross-talks with JH signaling by suppressing Met and gce expression.
abstract: Juvenile hormone (JH) plays key roles in controlling insect growth and metamorphosis. However, relatively little is known about the JH signaling pathways. Until recent years, increasing evidence has suggested that JH modulates the action of 20-hydroxyecdysone (20E) by regulating expression of broad (br), a 20E early response gene, through Met/Gce and Kr-h1. To identify other genes involved in JH signaling, we designed a novel Drosophila genetic screen to isolate mutations that derepress JH-mediated br suppression at early larval stages. We found that mutations in three Wnt signaling negative regulators in Drosophila, Axin (Axn), supernumerary limbs (slmb), and naked cuticle (nkd), caused precocious br expression, which could not be blocked by exogenous JHA. A similar phenotype was observed when armadillo (arm), the mediator of Wnt signaling, was overexpressed. qRT-PCR revealed that Met, gce and Kr-h1expression was suppressed in the Axn, slmb and nkd mutants as well as in arm gain-of-function larvae. Furthermore, ectopic expression of gce restored Kr-h1 expression but not Met expression in the arm gain-of-function larvae. Taken together, we conclude that Wnt signaling cross-talks with JH signaling by suppressing transcription of Met and gce, genes that encode for putative JH receptors. The reduced JH activity further induces down-regulation of Kr-h1expression and eventually derepresses br expression in the Drosophila early larval stages.
authors.affiliation: Department of Entomology, University of Maryland at College Park, College Park, Maryland, United States of America.
authors.forename: Mohamed
authors.initials: M
authors.lastname: Abdou
authors.forename: Cheng
authors.initials: C
authors.lastname: Peng
authors.forename: Jianhua
authors.initials: J
authors.lastname: Huang
authors.forename: Ola
authors.initials: O
authors.lastname: Zyaan
authors.forename: Sheng
authors.initials: S
authors.lastname: Wang
authors.forename: Sheng
authors.initials: S
authors.lastname: Li
authors.forename: Jian
authors.initials: J
authors.lastname: Wang
mesh_terms: D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins / Q000037:antagonists & inhibitors / Q000235:genetics*; D004330:Drosophila / Q000235:genetics* / Q000378:metabolism; D029721:Drosophila Proteins / Q000037:antagonists & inhibitors / Q000235:genetics*; D005786:Gene Expression Regulation; D007605:Juvenile Hormones / Q000378:metabolism*; D051741:Kruppel-Like Transcription Factors / Q000235:genetics; D007814:Larva / Q000378:metabolism; D020239:Receptor Cross-Talk / Q000502:physiology; D014157:Transcription Factors / Q000037:antagonists & inhibitors / Q000235:genetics*; D014158:Transcription, Genetic; D060449:Wnt Signaling Pathway / Q000502:physiology*
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D029721:Drosophila Proteins; D007605:Juvenile Hormones; D051741:Kruppel-Like Transcription Factors; D014157:Transcription Factors; C497242:Kr-h1 protein, Drosophila; C111234:MET protein, Drosophila; C543965:gce protein, Drosophila
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