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Although endocrine changes are known to modulate the timing of major developmental transitions, the genetic mechanisms underlying these changes remain poorly understood. In insects, two developmental hormones, juvenile hormone (JH) and ecdysteroids, are coordinated with each other to induce developmental changes associated with metamorphosis. However, the regulation underlying the coordination of JH and ecdysteroid synthesis remains elusive. Here, we examined the function of a homolog of the vertebrate POU domain protein, Ventral veins lacking (Vvl)/Drifter, in regulating both of these hormonal pathways in the red flour beetle,  Tribolium castaneum  (Tenebrionidae). RNA interference-mediated silencing of  vvl  expression led to both precocious metamorphosis and inhibition of molting in the larva. Ectopic application of a JH analog on  vvl  knockdown larvae delayed the onset of metamorphosis and led to a prolonged larval stage, indicating that Vvl acts upstream of JH signaling. Accordingly,  vvl  knockdown also reduced the expression of a JH biosynthesis gene,  JH acid methyltransferase 3  ( jhamt3 ). In addition, ecdysone titer and the expression of the ecdysone response gene,  hormone receptor 3  ( HR3 ), were reduced in  vvl  knockdown larvae. The expression of the ecdysone biosynthesis gene  phantom  ( phm ) and  spook  ( spo ) were reduced in  vvl  knockdown larvae in the anterior and posterior halves, respectively, indicating that Vvl might influence ecdysone biosynthesis in both the prothoracic gland and additional endocrine sources. Injection of 20-hydroxyecdysone (20E) into  vvl  knockdown larvae could restore the expression of  HR3  although molting was never restored. These findings suggest that Vvl coordinates both JH and ecdysteroid biosynthesis as well as molting behavior to influence molting and the timing of metamorphosis. Thus, in both vertebrates and insects, POU factors modulate the production of major neuroendocrine regulators during sexual maturation.

The POU Factor Ventral Veins Lacking/Drifter Directs the Timing of Metamorphosis through Ecdysteroid and Juvenile Hormone Signaling