Biology Reference
In-Depth Information
of
upd2
levels. This may be explained by remodeling of the metabolic pro-
gram by using fat or carbohydrates as an energy source. Importantly, this
finding highlights that not only proteins, but also dietary sugar and fat affects
systemic insulin signaling and may be important for the regulation of ecdy-
sone production and developmental timing.
Stimulation of systemic growth by the fat body also seems to depend on the
protein synthesis rate within the fat body. It was recently shown that Maf1, a
repressor of RNA polymerase III mediated tRNA synthesis, is involved in
nutrient dependent regulation of growth and developmental timing
(
Marshall, Rideout, & Grewal, 2012; Rideout et al., 2012
). In nutrient rich
conditions, TOR-dependent inhibition of Maf1 in the fat body promotes
tRNA synthesis in this tissue, which increases growth at the organismal level
by stimulating brain-derived
DILP2
and
DILP5
transcription. This provides
additional evidence for the fat-to-brain axis and the importance of fat
body-derived secreted factors in regulating insulin secretion from the IPCs.
Interestingly, suppressing
Maf1
specifically in the fat body, but not muscle
or brain, is sufficient to accelerate pupariation. tRNA
i
Met
is an important target
of Maf1 and increasing the dose of
tRNA
i
Met
phenocopies the inhibition of
Maf1 in the fat body. This suggests a model inwhich this single tRNA, impor-
tant for initiation of translation, is a limiting factor for protein synthesis and
plays a key role in fine-tuning growth and timing of ecdysone release in
response to diet.
The fat body itself has also been shown to be a source of insulin as it is the
predominant site of
DILP6
expression, which is increased by ecdysone and
during starvation (
Okamoto et al., 2009; Slaidina, Delanoue, Gronke,
Partridge, & Leopold, 2009
). In contrast to the DILPs derived from the brain,
DILP6 sustains growth during the non-feeding pupal stages. As the major
source of stored energy, the fat body is able to sustain levels of hemolymph
nutrients from initiation of autophagy during nutrient deprivation which is
otherwise suppressed by TOR signaling (
Oldham, 2011
). Furthermore,
nutrient dependent fat body signaling also induces
DILP
expression in glia cells
which promotes local proliferation and growth of neural stem cells (
Chell &
Brand, 2010
). Activation of TOR in the fat body is required to produce a
secreted signal that reactivates quiescent neuroblasts. This reactivation relies
on insulin/PI3K/TOR signaling in the neuroblast, but is independent of
the IPC-derived circulating DILPs that regulate systemic growth. Instead,
reactivation is a result of diet-dependent
DILP2
and
DILP6
expression in glia
cells that specifically reactivates neuroblast without affecting systemic growth.
The fact that the secreted fat body signal that stimulates glia
DILP2
and
DILP6
