title: Insulin signaling is necessary for vitellogenesis in Drosophila melanogaster independent of the roles of juvenile hormone and ecdysteroids: female sterility of the chico1 insulin signaling mutation is autonomous to the ovary.
abstract: It has been suggested that insulin signaling mutations of Drosophila melanogaster are sterile and long-lived because of juvenile hormone (JH) and ecdysteroid deficiency. However, female sterility of an insulin/IGF-like signaling mutant (chico(1)) of D. melanogaster is not mediated by downstream systemic signaling in terms of major alterations in JH or ecdysteroid levels. chico(1) is a null mutation in the insulin substrate protein (CHICO) gene of D. melanogaster. Homozygous chico(1) females are sterile and their oocytes do not mature beyond the last previtellogenic stage. Homozygous chico(1) females exhibit approximately wild-type rates of JH biosynthesis, ovarian release of ecdysteroids and haemolymph ecdysteroid levels, suggesting that these two major hormone systems play no role in producing the sterility. Previtellogenic wild-type ovaries transplanted into homozygous chico(1) females underwent vitellogenesis, showing that systemic factors present in mutant females are sufficient to support normal vitellogenesis. chico(1) ovaries transplanted into wild-type females did not undergo vitellogenesis indicating that CHICO is necessary in the ovary for vitellogenic maturation. The ovary transplant experiments corroborate the endocrine results and demonstrate that insulin/insulin-like signaling (IIS) is necessary for vitellogenesis even when sufficient levels of JH, ecdysteroids or other factors are present.
authors.affiliation: Department of Biology, Susquehanna University, Selinsgrove, PA 17870, USA.
authors.forename: David S
authors.initials: DS
authors.lastname: Richard
authors.forename: Robert
authors.initials: R
authors.lastname: Rybczynski
authors.forename: Thomas G
authors.initials: TG
authors.lastname: Wilson
authors.forename: Yue
authors.initials: Y
authors.lastname: Wang
authors.forename: Marta L
authors.initials: ML
authors.lastname: Wayne
authors.forename: You
authors.initials: Y
authors.lastname: Zhou
authors.forename: Linda
authors.initials: L
authors.lastname: Partridge
authors.forename: Lawrence G
authors.initials: LG
authors.lastname: Harshman
mesh_terms: D000818:Animals; D049628:Body Size; D029721:Drosophila Proteins / Q000235:genetics / Q000502:physiology*; D004331:Drosophila melanogaster / Q000235:genetics / Q000502:physiology*; D026461:Ecdysteroids / Q000502:physiology; D005260:Female; D006579:Heterozygote; D006720:Homozygote; D007328:Insulin / Q000502:physiology*; D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000502:physiology*; D007605:Juvenile Hormones / Q000502:physiology; D009154:Mutation; D010053:Ovary / Q000502:physiology; D015398:Signal Transduction; D014818:Vitellogenesis / Q000502:physiology*
chemical_list: D029721:Drosophila Proteins; D026461:Ecdysteroids; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins; D007605:Juvenile Hormones; C120233:chico protein, Drosophila