Regulation of critical weight in the tobacco hornworm, Manduca sexta


Meeting Abstract

129.6  Tuesday, Jan. 7 14:45  Regulation of critical weight in the tobacco hornworm, Manduca sexta. HATEM, N.E.**; SUZUKI, Y.; Wellesley College; Wellesley College nhatem@wellesley.edu

The regulation of the timing metamorphosis is a critical event in many organisms. In insects, a size assessment point called the critical weight marks the time at which metamorphosis is no longer delayed even when animals are starved. The timing of metamorphosis in the tobacco hornworm, Manduca sexta, is primarily regulated by juvenile hormone (JH). During the final instar, metamorphosis is inhibited by JH until the larva reaches the critical weight when JH titers drop. In contrast, studies have shown that in the fruit fly Drosophila melanogaster, the critical weight is regulated by nutrition-dependent insulin signaling in the prothoracic gland, the major site of ecdysteroid biosynthesis. Alterations of prothoracic gland size through the manipulation of insulin signaling lead to shifts in the critical weight. In this study, we examined the role of insulin/TOR signaling in the determination of the critical weight in Manduca. By feeding Manduca rapamycin treated diets, we inhibited TOR signaling in final instar larvae, and the effect on the critical weight was examined. In wildtype larvae, the peak size was unaffected when fed rapamycin although the growth rate was reduced. Critical weight was also unaffected when fed rapamycin. However, the size of the prothoracic gland at the critical weight was disproportionately smaller in larvae fed rapamycin. These results indicate that insulin/TOR signaling does not play a major role in the determination of critical weight in wildtype Manduca. Thus, JH overrides the nutritionally dependent critical weight regulation in this species. Our study shows that the critical weight is regulated by two distinct mechanisms, one that senses body size (mediated by JH) and another that senses nutritional input (mediated by insulin/TOR signaling). The relative contribution of these two mechanisms therefore determines whether body size or nutritional availability determines the timing of metamorphosis.

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