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is largely decoupled from nutrients, the fat body responds rapidly to changes
in the internal milieu (
Britton & Edgar, 1998
). Inhibiting amino acid trans-
port, and thus, TOR signaling in the fat body is sufficient to delay metamor-
phosis and nonautonomously reduce insulin signaling and systemic growth
(
Colombani et al., 2003
). Recently, it was found that nutrient mediated
inhibition of Maf1, a repressor of RNA polymerase III-dependent tRNA
transcription, in the fat body nonautonomously increases growth and accel-
erates pupariation (
Rideout et al., 2012
). Inhibition of Maf1 is TOR depen-
dent and promotes transcription of tRNA
Met
which is a limiting factor for
protein synthesis in the fat body that controls organismal growth and timing
of pupariation. Together, these results suggest that normal timing of meta-
morphosis is dependent on a positive signal from that fat body which is a
central tissue for coordinating nutrient availability with organismal growth
and timing of maturation.
The FDS appears to be a humoral factor(s) that conveys the fat body
amino acid status to the IPCs in the brain to regulate Dilp release
(
Geminard et al., 2009; Rideout et al., 2012
). Combined with observations
that insulin regulates ecdysone release from the PG (
Caldwell et al., 2005;
Colombani et al., 2005; Mirth et al., 2005
), it provides a mechanism for cou-
pling nutrient status information with ecdysone release (
Fig. 1.2
). Consistent
with this, increasing insulin signaling from the IPCs is sufficient to induce
premature ecdysone release and pupariation (
Walkiewicz & Stern, 2009
).
These studies agree with the fact that bombyxin, an insulin-like peptide
from the silkworm
Bombyx mori
, was originally characterized for its ability
to stimulate ecdysone synthesis (
Kiriishi, Nagasawa, Kataoka, Suzuki, &
Sakurai, 1992; Nagasawa et al., 1986; Rybczynski, 2005
). Although insulin
stimulates PG cell growth, the effect on ecdysone synthesis appears to be
specific as growth inducers such as dMyc and cyclin D/Cdk4 increase PG
cell size, but not ecdysone synthesis (
Colombani et al., 2005
). Ecdysone pro-
duced in the PG also feeds back on the fat body to regulate organismal
growth (
Colombani et al., 2005; Delanoue, Slaidina, & Leopold, 2010
).
The TOR-dependent amino acid sensor that resides in the larval fat body
cells may ensure that after each molt a certain amount of nutrient-dependent
growth is required to reset the “developmental timer.” This checkpoint
ensures a minimal period of feeding before the PG becomes competent
to produce an ecdysone pulse. Considering that insulin probably plays a cen-
tral role in relaying the critical weight signal, the fat body sensor may be a key
parameter in critical weight assessment. Accumulating evidence suggests that
the fat body with its metabolic and endocrine activities (
Britton & Edgar,
