Endocrine control of ecdysteroid and juvenile hormone production
L. I. Gilbert
Dept. of Biology,
Univ. of N. Carolina, Campus Box #3280 Coker Hall, Chapel Hill, NC
27599-3280, USA
New data will be
discussed on the means by which the prothoracicotropic hormone (PTTH)
of Manduca sexta stimulates the prothoracic glands to
synthesize and release 3-dehydroecdysone. The process is initiated
by PTTH-opening of a calcium channel leading to an increase in the
amount and activity of a number of protein kinases, one of which
has the capacity to enter the nucleus. The others, PKA and S6
kinase are utilized to phosphorylate S6 which is a protein
constituent of the ribosome and has important roles in modulating
protein synthesis, and in this case, for the purpose of
stimulating ecdysteroidogenesis. How the prothoracic glands are
turned off once the hemolymph ecdysteroid level has reached a peak
was answered by demonstrating changes in the isoforms of
ultraspiracle (usp) and the ecdysone receptor (EcR) which compose
a dimer. The studies reveal changes in particular isoforms when
the prothoracic glands are challenged both in vitro and in vivo.
By 20-hydroxyecdysone (20E). Since ecdysteroids may also have a
modulating role on the corpus allatum (source of juvenile
hormone), a series of studies was conducted with the ecdysone
receptor of the corpus allatum in vitro. The data showed that the
isoform composition was specifically and reproducibly changed in
the presence of 20E. There have been many reports in the
literature of JH stimulating or inhibiting the prothoracic glands
in vivo so that the rate of ecdysteroid synthesis is changed. This
view, for the most part, was based on experiments in vivo and it
was not proven unequivocally that JH affects the prothoracic
glands directly. Our studies on the Manduca prothoracic
glands indicate that it is indeed an indirect effect of JH on the
prothoracic glands eliciting the modulation of ecdysteroidogenesis.
Index terms:
molting, control of; second messengers; signal transduction; EcR (ecdysteroid
receptor).
Copyright: The copyrights of
this original work belong to the authors (see right-most box in
title table). This abstract appeared in Session 18 –
REPRODUCTION AND DEVELOPMENT Symposium and Poster Session,
ABSTRACT BOOK II – XXI-International Congress of Entomology,
Brazil, August 20-26, 2000.
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