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for stimulation of ecdysone biosynthesis in the PG during the postcritical
weight period, and so may not influence the two low-level ecdysone peaks
at 20 and 28 h after ecdysis to the third instar nor the subsequent high-level
peak at 44 h that is thought to trigger pupariation (
Warren et al., 2006
). In
fact, starvation after reaching critical weight, which is assumed to reduce
insulin signaling in the PG, actually slightly accelerates pupariation in
Drosophila
(
Mirth & Riddiford, 2007; Stieper et al., 2008
). Thus, insulin
signaling seems to be required for the first critical weight peak approximately
8 h after the L2/L3 transition. Increase in insulin signaling possibly informs
the endocrine system of the nutritional status of the larva. But how does the
system sense critical size? One possibility is that some threshold level of
insulin stimulates the biosynthetic pathway directly to produce the critical
weight ecdysone peak. Another possibility is that insulin makes the PG com-
mit to ecdysone synthesis by providing competence to other signals such as
PTTH which then dictates the timing of some, or perhaps all, of the
subsequent ecdysone peaks during the third instar. Under this view, insulin
signaling would not directly produce the critical weight peak. This is
consistent with the observation that insulin does not stimulate ecdysone
biosynthesis in
Manduca
(
Walsh & Smith, 2011
).
From one perspective, it seems more intuitive that pulses of PTTH
generate the precisely timed ecdysone peaks, instead of insulin. For example,
PTTH is a more potent inducer of ecdysone synthesis than insulin and is
released from neurons that directly innervate the PG (
McBrayer et al.,
2007; Rybczynski, 2005
). Transcription of
PTTH
exhibits ultradian period-
icity during the third instar (
McBrayer et al., 2007
), also making PTTH a
likely candidate for a periodic ecdysone pulse generator. Recently,
nucleocytoplasmic trafficking of the nuclear receptor DHR4 in the PG
was shown to be PTTH dependent (
Ou et al., 2011
). Lack of PTTH or
torso
disrupts the first nucleocytoplasmic transition 4 h after the L2/L3 transition.
This implies that PTTH signaling indeed occurs in advance to the critical
weight peak. A second low-level ecdysone peak 90 h AEL is associated with
a change in glue gene expression that allows the puparium to adhere to its
substrate. The third low-level ecdysone peak 98 h AEL is associated with
wandering behavior and the cessation of feeding. Consistent with this,
reduced ecdysone levels results in a prolonged feeding period, delayed
wandering and asynchrony of the ecdysone gene response (
McBrayer et al.,
2007; Rewitz, Yamanaka, et al. 2009
).
If the role of insulin is to endow the PG with competence to produce
ecdysone in response to PTTH, it would have to interact with a central
