Molecular mechanisms of cuticular melanization in the tobacco hornworm, Manduca sexta (L.) (Lepidoptera : Sphingidae)

Abstract

The absence of juvenile hormone (JH) around the time of head capsule slippage (HCS) causes cuticular melanization in Manduca sexta (Lepidoptera : Sphingidae) larvae. The epidermis begins to produce a granular phenoloxidase (PO) as a proenzyme a few hours after HCS; then the enzyme is incorporated into the newly synthesized cuticle in the form of premelanin granules. A neuroendocrine factor from the abdominal nerve cord is necessary for the deposition of the granules. This PO in the granules is activated as a result of the decline in ecdysteroid titer at the end of the molt. Dopamine, the precursor for melanin, is produced by the epidermis at the end of the molt, due to an increase in dopa decarboxylase (DDC) which catalyzes its conversion from dopa. DDC levels are 2-fold higher in melanizing JH-deficient larvae. The rise in DDC activity is controlled at the transcriptional level and dependent on the changing ecdysteroid titer during the molt. DDC transcription is programmed during the molting rise in ecdysteroids, and does not begin until the titer falls below a critical level. 20-Hydroxyecdysone was found to cause the synthesis of a short-lived transcription factor(s) which binds to the promoter region of the DDC gene and suppresses transcription.