title: Cricket body size is altered by systemic RNAi against insulin signaling components and epidermal growth factor receptor.
abstract: A long-standing problem of developmental biology is how body size is determined. In Drosophila melanogaster, the insulin/insulin-like growth factor (I/IGF) and target of rapamycin (TOR) signaling pathways play important roles in this process. However, the detailed mechanisms by which insect body growth is regulated are not known. Therefore, we have attempted to utilize systemic nymphal RNA interference (nyRNAi) to knockdown expression of insulin signaling components including Insulin receptor (InR), Insulin receptor substrate (chico), Phosphatase and tensin homologue (Pten), Target of rapamycin (Tor), RPS6-p70-protein kinase (S6k), Forkhead box O (FoxO) and Epidermal growth factor receptor (Egfr) and observed the effects on body size in the Gryllus bimaculatus cricket. We found that crickets treated with double-stranded RNA (dsRNA) against Gryllus InR, chico, Tor, S6k and Egfr displayed smaller body sizes, while Gryllus FoxO nyRNAi-ed crickets exhibited larger than normal body sizes. Furthermore, RNAi against Gryllus chico and Tor displayed slow growth and RNAi against Gryllus chico displayed longer lifespan than control crickets. Since no significant difference in ability of food uptake was observed between the Gryllus chico(nyRNAi) nymphs and controls, we conclude that the adult cricket body size can be altered by knockdown of expressions of Gryllus InR, chico, Tor, S6k, FoxO and Egfr by systemic RNAi. Our results suggest that the cricket is a promising model to study mechanisms underlying controls of body size and life span with RNAi methods.
authors.affiliation: Department of Life Systems, Institute of Technology and Science, The University of Tokushima, Tokushima, Japan.
authors.forename: Noha
authors.initials: N
authors.lastname: Dabour
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Bando
authors.forename: Taro
authors.initials: T
authors.lastname: Nakamura
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Miyawaki
authors.forename: Taro
authors.initials: T
authors.lastname: Mito
authors.forename: Hideyo
authors.initials: H
authors.lastname: Ohuchi
authors.forename: Sumihare
authors.initials: S
authors.lastname: Noji
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D049628:Body Size; D003001:Cloning, Molecular; D066246:ErbB Receptors / Q000235:genetics / Q000378:metabolism*; D005260:Female; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D017344:Genes, Insect; D006135:Gryllidae / Q000235:genetics / Q000254:growth & development* / Q000378:metabolism; D019476:Insect Proteins / Q000235:genetics / Q000378:metabolism; D007328:Insulin / Q000378:metabolism*; D008136:Longevity; D008297:Male; D008969:Molecular Sequence Data; D009758:Nymph / Q000235:genetics / Q000254:growth & development / Q000378:metabolism; D034622:RNA Interference; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism
chemical_list: D051858:Forkhead Transcription Factors; D019476:Insect Proteins; D007328:Insulin; D066246:ErbB Receptors; D011972:Receptor, Insulin; D058570:TOR Serine-Threonine Kinases