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is the primary mechanism for coordinating nutrient uptake with ecdysone
synthesis. Nevertheless, inhibition of TOR signaling in the PG reduces
ecdysone synthesis and delays pupariation. This implies that cellular levels
of amino acids regulate the steroidogenic activity of the PG and/or that
TOR is cross-activated by the insulin pathway. The insulin/TOR pathway
may also crosstalk with the MAPK pathway downstream of PTTH or they
may converge on common targets to promote ecdysone synthesis as reported
in other systems ( Mendoza, Er, & Blenis, 2011 ). The nutrition-dependent
checkpoint for ecdysone biosynthesis may potentially also be controlled
by a direct response of the PG to a fat body derived signal.
4. FINE-TUNING SYSTEMIC INSULIN SIGNALING
4.1. Antagonistic interactions between ecdysone
and insulin
While peaks of ecdysone promote transitions between developmental stages
and eventually the onset of pupariation, basal levels of ecdysone produced
and released from the PG negatively regulates insulin mediated growth
( Boulan et al., 2013; Colombani et al., 2005; Delanoue, Slaidina, &
Leopold, 2010; Francis, Zorzano, & Teleman, 2010 ). Stimulation of insulin
signaling in most cases promotes growth, however, PG-specific activation of
insulin signaling reduces final body size and vice versa ( Caldwell et al., 2005;
Colombani et al., 2005; Mirth et al., 2005 ). A recent report shows that
insulin signaling modulates the basal level of ecdysone synthesis in the
PG by repressing bantam , a microRNA that suppresses ecdysone synthesis
( Boulan et al., 2013 ). These studies suggest that insulin regulates basal ecdy-
sone levels, which makes it possible that insulin signaling is not involved in
the production of the ecdysone pulses during L3. Since ecdysone inhibits
growth by influencing the ecdysone receptor (EcR) activity in the fat body
leading to a systemic reduction of insulin signaling ( Fig. 2.3 ) this may be a
way to adjust growth to the internal nutritional state. Removal of EcR func-
tion in this tissue, but not other organs, increases growth and final pupal size
without affecting developmental time ( Colombani et al., 2005; Delanoue
et al., 2010 ). The transcription factor dMyc appears to be a specific target
of EcR in the fat body, since downregulation of dMyc in the fat body is suf-
ficient to mediate the systemic inhibitory effect of ecdysone. Ecdysone acts
by inhibiting dMyc in the fat body which leads to nonautonomous suppres-
sion of growth ( Delanoue et al., 2010; Grewal, 2009 ). This further supports
the notion that the fat body is a central relay secreting factors into the
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