Topical application of 400 micro g of the juvenile hormone analog, methoprene, to females of the penultimate instar of Leucophaea maderae failed to induce vitellogenin synthesis. However, last instar females showed an increasing response level in making vitellogenin as they aged during the first half of the instar. In the second half of the last instar the response to methoprene declined to nearly zero when the prothoracic glands have become highly active. Then, a few days before the metamorphic molt the responsiveness reached maximal levels, i.e., comparable to adult females. These data suggest that the fat body develops competency to produce vitellogenin during the last nymphal instar, but increasing titers of ecdysone then interfere with the action of methoprene and consequently production of vitellogenin is curtailed. When prothoracic glands from the second half of the last instar were implanted into adult females, the normal activation of the corpora allata, or their accelerated activation induced by mating, did not occur. Likewise, an activation of the corpora allata due to the severance of the NCCI was not observed when prothoracic glands had been implanted prior to such operations. Thus, ecdysone released by the prothoracic glands appeared to directly inhibit the isolated corpora allata in vivo i.e. without the mediation by the brain. Methoprene applied to allatectomized adult females induced vitellogenin synthesis in a dose dependent manner. This induction was, however, quantitatively reduced by implanted active prothoracic glands, particularly when low doses of methoprene had been applied. Methoprene higher than 5 micro g overcame the inhibitory potency of the implanted prothoracic glands. The effect of the prothoracic glands, i.e. ecdysone, appears to signal an interference with the action of methoprene at the target tissues, the fat body. The exposure of the fat body to a given juvenile hormone/ecdysone ratio dictates the apparent effectiveness of ecdysone. The precise mode of the interaction of juvenile hormone and ecdysone on the adult fat body is not known. These data show that ecdysone inhibits vitellogenesis by two independent mechanisms: 1) inhibition of the corpora allata resulting in the inhibition of juvenile hormone production and 2) inhibition of vitellogenin synthesis by the fat body. Both of these mechanisms appear to be operative in immature and mature animals. However, the action of ecdysones on the fat body is only seen after it had acquired competency to make vitellogenin during the last nymphal instar.