Biology Reference
In-Depth Information
Insulin
Activin
PTTH
To r s o
Babo
Punt
InR
Smad2
cross
talk
PI3K
Ras
Erk
AKT
Ecdysone
DHR4
TSC1
TSC2
Nutrients
b
FTZ-F1
E75
JH
TOR
Broad
DHR3
NOS
?
Figure 1.3 Mechanisms converging on the PG time ecdysone production. TGF
/Activin
is required for normal expression of the insulin receptor (InR) and torso, which provides
glandular competence to PTTH (developmental) and insulin (nutrient) cues. Further-
more, the PG harbors a TOR-dependent nutrients sensor that presumably allows com-
pensation for poor nutrient environments. Under such conditions, ecdysone release is
delayed which prolongs the growth period. Broad is required for normal expression of
the Halloween genes encoding the enzymes mediating ecdysone synthesis, although it
is not clear if JH regulates broad in the PG. Nitric oxide (NO) generated by the nitric oxide
synthase (NOS) regulates nuclear receptor signaling in the PG. In turn, NO inhibits E75, a
repressor of DHR3 which then activates expression of
b
FTZ-F1, a nuclear receptor
required for expression of at least two key ecdysone biosynthetic enzymes, Phantom
and Disembodied.
b
that insulin/TOR also has a direct role in regulating ecdysone synthesis in
the PG (
Caldwell et al., 2005; Colombani et al., 2005; Gibbens et al., 2011;
Layalle et al., 2008; Mirth et al., 2005
). Under this view, the developmental
timer in the PG is informed of the nutritional status via insulin/TOR to
adjust ecdysone synthesis (
Fig. 1.3
). Although the role insulin plays in the
production of the ecdysone peaks is not clear, as described insulin is likely
involved in setting the critical weight parameter that commits the PG to
ecdysone biosynthesis. Assessment of the temporal requirement for insulin
during development has demonstrated that reduced insulin signaling delays
timing of pupariation before, but not after, the critical weight checkpoint
(
Shingleton et al., 2005
). This implies that insulin signaling is not important
