Meeting Abstract
P1.160 Saturday, Jan. 4 15:30 The role of the POU factor Ventral veins lacking in the regulation of metamorphosis initiation KO, A*; CHENG, C; CHAIEB, L; KOYAMA, T; MIRTH, C.K.; SMITH, W.A.; SUZUKI, Y; Wellesley College; Wellesley College; Wellesley College; Instituto Gulbenkian de Ciência; Instituto Gulbenkian de Ciência; Northeastern University; Wellesley College ysuzuki@wellesley.edu
Metamorphosis and puberty are characterized by dramatic morphological and behavioral changes, and their regulation and evolution continues to be a puzzling scientific enigma. In insects, the timing of metamorphosis is regulated by the interaction between juvenile hormone (JH) and ecdysteroids. Here we show that the POU transcription factor Ventral vein lacking (Vvl) plays an important role in regulating the onset of metamorphosis. Silencing Vvl expression using RNAi interference (RNAi) resulted in the induction of precocious metamorphosis in Tribolium castaneum and a reduction in the expression of the JH-inducible gene kruppel homolog 1 (kr-h1). Topical application of JH on individuals lacking Vvl delayed the onset of metamorphosis and rescued the normal expression of kr-h1, indicating that JH levels are reduced in vvl RNAi animals. Furthermore, the expression of the JH biosynthesis enzyme coding gene jh acid methyltransferase 3 also decreased with vvl knockdown. Interestingly, in addition to inducing precocious metamorphosis, molting was also inhibited in vvl RNAi animals. Since molting is regulated by ecdysteroids, the activity of ecdysteroid signaling pathway was examined in vvl knockdown animals. Consistent with this hypothesis, ecdysone response gene expression was decreased in vvl RNAi animals. Vvl was also found to interact with Ecdysone receptor and its heterodimeric partner, Ultraspiracle. Finally, ecdysone titers were lower in vvl knockdown animals. Thus, Vvl influences both JH and ecdysone signaling and biosynthesis, potentially acting as an integrator of both hormonal pathways to regulate the metamorphic onset.
