期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2003
卷号：100
期号：23
页码：13338-13343
DOI：10.1073/pnas.2234416100
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：In anautogenous mosquitoes, vitellogenesis, which includes production of yolk protein precursors, requires blood feeding. Consequently, mosquitoes transmit many diseases. Understanding the molecular mechanisms of vitellogenesis regulation will contribute significantly to vector control strategies. Newly emerged Aedes aegypti females require 3 days before becoming competent to activate vitellogenesis in response to a blood-meal-initiated, elevated titer of 20-hydroxyecdysone (20E). An orphan nuclear receptor gene {beta}FTZ-F1 is transcribed in the fat body of newly emerged mosquito females; however, the {beta}FTZ-F1 protein is only found 3 days later. Dramatically increased titer of the juvenile hormone III (JH III) is essential for the acquisition of 20E competence. In vitro fat body culture experiments have shown that {beta}FTZ-F1 protein appears after exposure to JH III. Injection of double-stranded RNA complementary to {beta}FTZ-F1 into newly emerged females attenuated expression of the early genes EcR-B, E74B, and E75A and the target YPP gene Vg, in response to a blood meal. Thus, {beta}FTZ-F1 is indeed the factor defining the acquisition of competence to 20E in the mosquito fat body. Moreover, this is achieved through JH III-mediated posttranscriptional control of {beta}FTZ-F1.
