Biology Reference
In-Depth Information
The responsiveness of the CA to ecdysteroid declines as a function of
development after the last larval ecdysis and disappears completely by
60 h when synthetic activity is shut off (
Kaneko, Kinjoh, et al., 2011
). It
must be noted that concentrations of ecdysteroid as low as 30 ng/ml strongly
stimulate JH biosynthesis, indicating that the presence of even a low concen-
tration of ecdysteroid is enough to maintain JH biosynthesis; therefore, the
decline of ecdysteroid titer after the last larval ecdysis is one of the key events
leading to the cessation of JH biosynthesis at this time (
Fig. 3.3
A).
At the time of the declining ecdysteroid titer, the mRNA levels of most
of the JH synthetic enzymes in the CA gradually declined (
Kinjoh et al.,
2007
;
Fig. 3.1
B). The presence of ecdysteroid prevented these declines,
while mRNAs for both
JHAMT
and HMG-CoA reductase (
HMGR
) were
stimulated as JH synthesis became high, so that the stimulation of JH
synthesis was primarily due to the activation of JHAMT, one of the rate-
limiting enzymes in
Bombyx
(T. Kinjoh & K. Hiruma, unpublished data;
Fig. 3.4
A), and also HMGR.
The activation of the CA by 20E requires nervous connections with the
brain, as 20E only activates JH synthesis by the CA when a brain-CC-CA
complex was intact (
Kaneko, Kinjoh, et al., 2011
). How the brain acts on the
CA is unknown, but whatever the mechanisms involved, the expression of
JH biosynthetic enzymes appears to be indirectly regulated by 20E. Unlike
the inhibitory action of a high concentration of ecdysteroid on JH synthesis
in the fourth instar larvae, RNAi suppression of E75 had little effect on the
stimulative action of ecdysteroid on
JHAMT
expression in the early fifth
stage larvae (Kinjoh & Hiruma, unpublished data), supporting the hypoth-
esis of indirect ecdysteroid action on the CA (
Fig. 3.4
A).
Thus, in very early fifth stage
Bombyx
larvae, the brain responds to the
postecdysial decline of ecdysteroid titer and signals to the CA via nervous
connections to change JH biosynthetic enzymes so as to shut off JH
biosynthesis (
Figs. 3.3
A and
3.4
A).
2.3. Regulation by neurotransmitters
Neurotransmitters, in particular biogenic amines, have been thought to
regulate JH, as maintaining intact nervous connections between the brain
and the CA affects JH synthesis (
Goodman & Granger, 2005; Granger,
Sturgis, Ebersohl, Geng, & Sparks, 1996
). Some biogenic amines such as
octopamine,
L
-glutamate, and dopamine have been shown to stimulate JH
synthesis by the isolatedCA
in vitro
.Here,we summarize howtwowell-studied
amines, dopamine and glutamate, act to regulate JH synthesis in the CA.
