Direct effects of hypoxia and nitric oxide on ecdysone secretion by insect prothoracic glands

Insect metamorphosis is controlled by the primary molting hormone ecdysone, which is secreted by the prothoracic glands (PG) to sequentially promote commitment of fifth (final) larval stage Manduca sexta larvae to pupae and then to adult development. A recent study suggests that low tissue oxygenation comprises the size sensing mechanism responsible for triggering molt timing in Manduca. In Drosophila, nitric oxide (NO) signaling appears to be required for normal developmental timing by influencing transcription of βFTZ-F1, a regulator of ecdysone production and metamorphic tissue progression. Furthermore, low intracellular oxygen supplies have been shown to enhance NO signaling cascades. Therefore, we set out to directly examine the effects of hypoxia (2% oxygen) and NO on ecdysone secretion and on ecdysone-promoting transcription factors using fifth larval stage Manduca PG. Our results suggest that oxygen and NO modify the steroidogenic capacity and sensitivity of the PG rather than directly stimulate ecdysone secretion.