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the fat body-derived nutritional signal. If this signal directly regulates the IPCs
or other classes of neurons that control the activity of the IPCs is not known.
Cell-autonomous nutrient sensing that controls the release of adipokinetic
hormone, the functional equivalent of the mammalian glucagon, does not
seem to operate in the insulin release control (
Kim&Rulifson, 2004
). Instead,
insulin secretion is controlled by PKA/CREB and ERK activity stimulated by
short neuropeptide F (sNPF) or other neuropeptides and neurotransmitters
such as serotonin and GABA (
Birse, Soderberg, Luo, Winther, & Nassel,
2011; Enell, Kapan, Soderberg, Kahsai, & Nassel, 2010; Kaplan,
Zimmermann, Suyama, Meyer, & Scott, 2008; Lee et al., 2008; Luo,
Becnel, Nichols, & Nassel, 2012; Walkiewicz & Stern, 2009
). Inhibition of
PKA/CREB in the IPCs increases insulin signaling and results in premature
ecdysone production and metamorphosis. Conversely, animals with ablated
IPCs and mutants with increased serotonin levels that inhibit insulin release
from the IPCs have reduced growth rates and delayed pupariation (
Kaplan
et al., 2008; Rulifson et al., 2002
). This shows that neural circuits as well as
endocrine mechanisms, such as the FDS, that regulate insulin release from
the IPCs are important for the control of ecdysone production. Insulin likely
acts directly on the PG (see below); in fact, the axons of the IPCs exit the brain
and release insulin from terminals on the anterior aorta and corpus cardiacum
close to the PG portion of the ring gland. It is also possible, however, that sys-
temic insulin acts on the nerve endings of the PG neurons to send a retrograde
signal that affects PTTH production. In general, the identity and mechanisms
by which both internal and environmental inputs control PTTH activity is
poorly understood, with perhaps the exception of photoperiodic inputs.
As found for lepidopterans, PTTH release in
Drosophila
appears to be
controlled by the photoperiod (
Fig. 1.2
), since the circadian clock neurons,
producing the pigment dispersing factor (PDF), impinge on the PG neurons
(
McBrayer et al., 2007; Siegmund & Korge, 2001
). The photoperiodic
gating of PTTH recurs daily but is presumably not “read” by the system until
passage through other checkpoints have verified that the larva has completed
enough growth (
Nijhout, 1981
). In
pdf
mutant larvae the periodicity
of PTTH transcription is disrupted and clock mutations alter developmen-
tal timing (
Kyriacou, Oldroyd, Wood, Sharp, & Hill, 1990; McBrayer
et al., 2007
), suggesting a circadian checkpoint regulating PTTH release.
In lepidopterans, the PTTH release event is downstream of critical weight
and the period between critical weight and PTTH secretion (determined by
the time required for JH clearance) is called the PTTH delay period (
Nijhout
& Williams, 1974a,1974b
). Interestingly, rearing
Drosophila
larvae with
increased insulin signaling in the PG under constant light decreases time
