Biology Reference
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competence or is required for constitutive expression of
torso
and
InR
.Another
interesting possibility is that TGF
b
/Activin signaling is linked to the effect of
the SUMOylation pathway, since it has also been demonstrated that knock-
down of the SUMO gene,
smt3
, in the PG arrests development in the L3
(
Talamillo et al., 2008
). In this regard, it is interesting to note that Medea,
the co-Smad that forms a complex with dSmad2, is a primary target of
SUMOylation (
Miles et al., 2008
).
4. SHAPING DISCRETE ECDYSONE PULSES
4.1. Feedback control of ecdysone production
In addition to the mechanisms that increase ecdysone synthesis, there must be
ways to shut down PG activity as well as inactivate and remove ecdysone
from circulation in order to produce the temporally defined pulses of ecdy-
sone. Thus, the endocrine system must be under feedback regulation and
receive inputs from its own target tissues (
Fig. 1.4
). This idea is consistent
with studies showing that ecdysone inhibits ecdysone synthesis in the PG
of lepidopterans (
Beydon & Lafont, 1983; Gilbert et al., 2002; Sakurai &
Williams, 1989
). Furthermore,
EcR
is expressed in the PG of
Drosophila
during the time when the larvae initiate pupariation (
Talbot, Swyryd, &
Hogness, 1993
). Long-term incubation of the PG in the presence of
ecdysone reduces the sensitivity to PTTH (
Gilbert, Song, & Rybczynski,
1997; Song & Gilbert, 1998
), which indicates that ecdysone likely down-
regulates
torso
or other components mediating PTTH signaling or
ecdysteroidogenesis.
Conversely, when the activity of the PG is low, ecdysone appears to
stimulate its own synthesis, a mechanism that can increase and amplify
the signal. Further amplification of the signal may occur through the EcR
autoregulatory loop, through which
EcR
induces its own expression
(
Koelle et al., 1991
). These observations suggest that ecdysone synthesis
in the PG is controlled by feedforward and feedback loops that rapidly
modulate the ecdysone titer and determine the temporal boundaries for
the pulses. Interestingly,
torso
expression is induced by ecdysone, indicating
a potential feedforward regulatory mechanism (
Young et al., 2012
). On the
other hand, PTTH stimulation decreases
torso
mRNA levels, suggesting a
desensitizing mechanism similar to that observed for InR (
Puig, Marr,
Ruhf, & Tjian, 2003
). Although some controversies exist about the role
of ecdysone in the PG (
Kozlova & Thummel, 2002; Yamanaka &
