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metabolism of the host, a deeper understanding of crosstalk between
microbes, metabolism, and growth will be important to elucidate how these
interactions may affect timing of maturation.
3.3. Crosstalk of nutrient signaling and neuroendocrine
control of maturation
The findings that insulin/TOR signaling in the PG regulates ecdysone syn-
thesis ( Boulan, Mart´n, & Mil´n, 2013; Caldwell et al., 2005; Colombani
et al., 2005; Layalle et al., 2008; Mirth et al., 2005 ) have provided a connec-
tion between ecdysone synthesis and nutrition. These studies demonstrate
that both pathways converge on the regulation of ecdysone synthesis in
the PG and suggest that the PG itself acts as a nutrient sensor to some extent.
Since insulin signaling only affects developmental time before critical weight
( Shingleton et al., 2005 ), it presumably plays a role in producing the first low-
level ecdysone pulse in the early L3, but not the subsequent peaks. If insulin is
directly responsible for the production of the low-level ecdysone pulse asso-
ciated with the critical weight switch, it requires that insulin is a regulator of
the ecdysone biosynthetic pathway, a view supported by the fact that
bombyxin, an insulin-like molecule, was first identified for its ability to stim-
ulate ecdysone biosynthesis in the silkworm Bombyx mori ( Nagasawa et al.,
1986 ). One possible mechanism is that a certain threshold level of insulin sig-
naling switches the PG to a nutrient independent program for the production
of ecdysone. An alternative explanation for the role of insulin in the PG is that
when insulin signaling passes a certain threshold it provides the PG with
competence to respond to other signals like PTTH that are then directly
responsible for producing the ecdysone pulses. Potential crosstalk between
the insulin and PTTH signaling pathways in the PG via MAPK/Erk also
opens the possibility that both signals are required simultaneously to produce
the critical weight ecdysone pulse. Another scenario is that insulin signaling
promotes PG cell growth and is permissive for ecdysone synthesis in the
gland, but that its direct coupling to the production of the ecdysone pulse
is upstream of PTTH. Some evidence suggests that PTTH is responsible
for producing the ecdysone peak associated with critical weight ( Ou,
Magico, & King-Jones, 2011; Rewitz & O'Connor, 2011 ). Insulin may
therefore potentially act directly or indirectly via the brain to control the
timing of PTTH release.
In addition to its response to insulin, the activity of TOR in the PG also
regulates ecdysone synthesis ( Layalle et al., 2008 ). This suggests that local
nutrient sensing occurs at the level of the PG, although it is unlikely that this
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