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 FTZ-F1 is transcribed in the fat body of newly emerged mosquito females; however, the 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 FTZ-F1 protein appears after exposure to JH III. Injection of double-stranded RNA complementary to 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, 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 FTZ-F1.I n oviparous animals, vitellogenesis is a key event in egg maturation, which involves the production of yolk protein precursors (YPPs) predominantly by extraovarial tissues and their uptake by developing oocytes. Numerous signals are involved in a precise coordination of vitellogenic tissues. In anautogenous mosquitoes, initiation of vitellogenesis requires a blood meal. As a consequence, mosquitoes are vectors of many devastating infectious diseases, including malaria, dengue fever, and lymphatic filariasis (1-4). Unraveling the molecular mechanisms of vitellogenesis regulation will aid the development of new strategies for more efficient vector control.In the yellow fever mosquito Aedes aegypti, blood feeding triggers a signaling cascade culminating in the elevation of titers of ecdysteroids, which is closely correlated with the production of YPPs in the fat body, a tissue functionally analogous to vertebrate liver (5-7). Also, the genes encoding two major YPPs, vitellogenin (Vg) and vitellogenic carboxypeptidase (VCP), are activated in fat bodies cultured in vitro on addition of the physiologically active ecdysteroid 20-hydroxyecdysone (20E), which suggests that the Vg and VCP genes are regulated by this hormone (8).The steroid hormone 20E controls larval molting and metamorphosis in many insects, and it functions during embryonic development and adult reproduction. The molecular mechanism of 20E action has been dissected in detail during Drosophila metamorphosis (9). As 20E titers are rising and dropping again, unique sets of genes are turned on and off at distinct stages. Additional factors are therefore essential for the achievement of such a precise control of gene expression. For instance, cuticle proteins, a major component of the insect exoskeleton, are...