Steroid signaling mediates nutritional regulation of juvenile body growth via IGF-binding protein in Drosophila
| Autor: | Seogang Hyun, Jin Ju Lim, Gangsik Han, Hyun Myoung Yun, Gang Jun Lee, Jaegeun Lee, Sujin Noh |
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| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine IGFBP7 medicine.medical_treatment Morphogenesis Adipose tissue Insulin-like growth factor-binding protein 03 medical and health sciences chemistry.chemical_compound Insulin resistance medicine Animals Nutritional Physiological Phenomena Multidisciplinary biology Growth factor Biological Sciences medicine.disease Cell biology Insulin-Like Growth Factor Binding Proteins Steroid hormone 030104 developmental biology chemistry Larva biology.protein Drosophila Female Steroids Ecdysone Signal Transduction |
| Zdroj: | Proceedings of the National Academy of Sciences. 115:5992-5997 |
| ISSN: | 1091-6490 0027-8424 |
| DOI: | 10.1073/pnas.1718834115 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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