Regulation of larval-larval molting and metamorphosis in the tobacco hornworm, Manduca sexta : roles of juvenile hormone, ecdysteroid and the brain /

In Manduca sexta, larval-larval molting of the IVth instar ensues in response to a large pulse of ecdysteroid. Ecdysone release by the prothoracic glands (PG), in turn, is stimulated by prothoracicotropic hormone (PTTH) from the brain. I show that juvenile hormone (JH) is necessary and its titer n...

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Bibliographic Details
Main Author: Lonard, David Michael
Format: Thesis Book
Language:English
Published: [Place of publication not identified] : [publisher not identified] ; 1996.
Subjects:
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Summary:In Manduca sexta, larval-larval molting of the IVth instar ensues in response to a large pulse of ecdysteroid. Ecdysone release by the prothoracic glands (PG), in turn, is stimulated by prothoracicotropic hormone (PTTH) from the brain. I show that juvenile hormone (JH) is necessary and its titer need not fall for PTTH release to occur. Application of the JH analog methoprene to larvae did not shift the hemolymph ecdysteroid titer profile nor did it affect PG activity in vitro. On the other hand, allatectomy abolished the ecdysteroid pulse which could be restored by application of methoprene. Neck-ligation and debraining experiments show that this effect of methoprene is mediated by the brain. In neck-ligated larvae, i.e., when PTTH is eliminated, the ecdysteroid hemolymph titer rises gradually and leads to a larval-pupal molt. In this situation, methoprene suppressed the ecdysteroid titer completely, possibly through direct inhibition of the PG. In the Vth instar, the process of metamorphosis is initiated when ecdysteroid release occurs in the absence of JH. The timing of the onset of metamorphosis is thought to be controlled by the brain through the release of PTTH which stimulates the release of the small "commitment" pulse of ecdysone by the PG. I provide evidence that compels modification of the current model of PTTH control of ecdysteroid production and titer at this time. These results also indicate that target tissues do not depend upon the absence of JH and presence of ecdysteroid to undergo metamorphosis. The brain is not necessary for an increase in ecdysteroid titer prior to metamorphosis and methoprene can also inhibit the production of ecdysteroid in brainless larvae. Furthermore, methoprene was unable to enforce the status quo of all features of the larval developmental program in intact larvae. In the methoprene treated larvae, metamorphosis of some tissues ensued in the absence of ecdysteroid but not in the absence of the brain, suggesting the existence of an effector of metamorphosis emanating from the brain which drives metamorphosis in addition to ecdysteroid. Regulation of ecdysone receptor MRNA levels in these larvae is also discussed.
Item Description:Vita.
"Major Subject: Biology".
Physical Description:ix, 100 leaves : illustrations ; 28 cm.
Issued also on microfiche from University Microfilms Inc.
Bibliography:Includes bibliographical references: pages 87-99.