Steroid signaling mediates nutritional regulation of juvenile body growth via IGF-binding protein in Drosophilaopen access
- Authors
- Lee, Gang Jun; Han, Gangsik; Yun, Hyun Myoung; Lim, Jin Ju; Noh, Sujin; Lee, Jaegeun; Hyun, Seogang
- Issue Date
- Jun-2018
- Publisher
- NATL ACAD SCIENCES
- Keywords
- juvenile growth; IIS/TOR signaling; steroid hormone; insulin-like growth factor-binding protein; Drosophila
- Citation
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.115, no.23, pp 5992 - 5997
- Pages
- 6
- Journal Title
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Volume
- 115
- Number
- 23
- Start Page
- 5992
- End Page
- 5997
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/2063
- DOI
- 10.1073/pnas.1718834115
- ISSN
- 0027-8424
1091-6490
- Abstract
- Nutritional condition during the juvenile growth period considerably affects final adult size. The insulin/insulin-like growth factor signaling (IIS)/target of rapamycin (TOR) nutrient-sensing pathway is known to regulate growth and metabolism in response to nutritional conditions. However, there is limited information on how endocrine pathways communicate nutritional information to different metabolic organs to regulate organismal growth. Here, we show that Imaginal morphogenesis protein-Late 2 (Imp-L2), a Drosophila homolog of insulin-like growth factor-binding protein 7 (IGFBP7), plays a key role in the nutritional control of organismal growth. Nutritional restriction during the larval growth period causes undersized adults, which is largely diminished by Imp-L2 mutation. We delineate a pathway in which nutritional restriction increases levels of the steroid hormone ecdysone, which, in turn, triggers ecdysone signaling-dependent Imp-L2 production from the fat body, a fly adipose organ, thereby attenuating peripheral IIS and body growth. Surprisingly, this endocrine pathway operates independent of the fat-body-TOR internal nutrient sensor, long believed to be the control center for nutrition-dependent growth. Our study reveals a previously unrecognized endocrine circuit mediating nutrition-dependent juvenile growth, which could also potentially be related to the insulin resistance frequently observed in puberty.
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