title: Disruption of insulin pathways alters trehalose level and abolishes sexual dimorphism in locomotor activity in Drosophila.
abstract: Insulin signaling pathways are implicated in several physiological processes in invertebrates, including the control of growth and life span; the latter of these has also been correlated with juvenile hormone (JH) deficiency. In turn, JH levels have been correlated with sex-specific differences in locomotor activity. Here, the involvement of the insulin signaling pathway in sex-specific differences in locomotor activity was investigated in Drosophila. Ablation of insulin-producing neurons in the adult pars-intercerebralis was found to increase trehalosemia and to abolish sexual dimorphism relevant to locomotion. Conversely, hyper-insulinemia induced by insulin injection or by over-expression of an insulin-like peptide decreases trehalosemia but does not affect locomotive behavior. Moreover, we also show that in the head of adult flies, the insulin receptor (InR) is expressed only in the fat body surrounding the brain. While both male and female InR mutants are hyper-trehalosemic, they exhibit similar patterns of locomotor activity. Our results indicate that first, insulin controls trehalosemia in adults, and second, like JH, it controls sex-specific differences in the locomotor activity of adult Drosophila in a manner independent of its effect on trehalose metabolism.
authors.affiliation: Equipe ATIPE: Bases Neurales du Mouvement chez la Drosophile, NAMC, CNRS, UMR-8620, Université Paris-Sud, Bâtiment 446, F-91405, Orsay, France.
authors.forename: Yesser Hadj
authors.initials: YH
authors.lastname: Belgacem
authors.forename: Jean-René
authors.initials: JR
authors.lastname: Martin
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D004330:Drosophila; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D005216:Fat Body / Q000378:metabolism; D005260:Female; D017353:Gene Deletion; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D007150:Immunohistochemistry / Q000379:methods; D051034:Inhibitor of Apoptosis Proteins / Q000235:genetics / Q000378:metabolism; D007301:Insect Hormones / Q000378:metabolism; D008297:Male; D008726:Methoprene / Q000494:pharmacology; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology*; D016296:Mutagenesis / Q000502:physiology; D011972:Receptor, Insulin / Q000235:genetics / Q000502:physiology*; D012727:Sex Characteristics; D012737:Sex Factors; D012726:Sexual Behavior, Animal; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology*; D013997:Time Factors; D014157:Transcription Factors / Q000235:genetics; D014199:Trehalose / Q000378:metabolism*
chemical_list: C111892:DIAP2 protein, Drosophila; D029721:Drosophila Proteins; D051034:Inhibitor of Apoptosis Proteins; D007301:Insect Hormones; D014157:Transcription Factors; C014956:adipokinetic hormone (locust); D008726:Methoprene; D014199:Trehalose; D011972:Receptor, Insulin