| Institution: | 1. Anhui Province Key Laboratory of Pollutant Sensitive Materials and Environmental Remediation, College of Life Sciences, Huaibei Normal University, Huaibei, China;2. Institute of Biomedicine, Jinan University, Guangzhou, China;3. Zhuhai Trinomab Biotechnology Co., Ltd., Zhuhai, China;4. Graduate School of Bio-Applications and Systems Engineering, Tokyo University of Agriculture and Technology, Tokyo, Japan;5. Key Laboratory of Animal Resistance Research, College of Life Science, Shandong Normal University, Jinan, China;6. Bioassay Research Department, Central Agricultural Pesticide Laboratory, Sabahia Plant Protection Research Station, Agricultural Research Center, Alexandria, Egypt;7. Institute of Plant Protection, Jiangsu Academy of Agricultural Sciences, Key Lab of Food Quality and Safety of Jiangsu Province-State Key Laboratory Breeding Base, Nanjing, China;1. BayerCropScience AG, 40789 Monheim, Germany;2. Department of Crop Protection, Faculty of Bioscience Engineering, Ghent University, Ghent, Belgium;3. Institute for Biodiversity and Ecosystems Dynamics, University of Amsterdam, Amsterdam, The Netherlands;1. Department of Genetics and Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, VIC 3052, Australia;2. School of Biological Sciences, University of Sydney, Sydney, NSW 2006, Australia;3. Australian Cancer Research Foundation Rational Drug Discovery Centre, St Vincent''s Institute of Medical Research, Fitzroy, VIC 3056, Australia;4. Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, VIC 3052, Australia |
| Abstract: | Adult development and production of up to 400 eggs within the pupal case of female silkmoths are both dependent on 20-hydroxyecdysone (20E), the steroid hormone of insects. When adult development was initiated with tebufenozide, the non-steroidal ecdysteroid agonist, instead of 20E, full development of all epidermal tissues like the wing was witnessed, but ovarian growth and egg formation was minimal. Administration of tebufenozide to female pharate adults caused disruption of the follicular epithelium, produced nurse cell damage, and inhibited oogenesis. Reduced ability to synthesize RNA and protein accompanied these tebufenozide induced morphological disturbances of the follicles. In vivo accumulation of vitellogenin (Vg) from the hemolymph was reduced in tebufenozide treated female ovaries as well as their ability to accumulate Vg in vitro. Determination of protein staining intensity and antibody reactivity of Vg pointed out that hemolymph Vg level remained fairly constant all through adult development whether induced by 20E or tebufenozide. Measurement of hemolymph volumes and hemolymph Vg levels of control and experimental animals allowed us to conclude that egg development involves the uptake of all the hemolymph proteins and not Vg alone. The loss of hemolymph that accompanies egg maturation was considerably reduced in tebufenozide initiated female pharate adults. 20E could not overcome ovarian growth inhibitory effects of tebufenozide. Dual mechanisms, one involving ecdysteroid antagonist action at the beginning of development, and the other unrelated to that function during heightened egg formation, are needed explain the biphasic inhibitory actions of tebufenozide on silkmoth ovaries. |
