Biology Reference
In-Depth Information
including the fat body that under such conditions mobilize stored energy to
maintain hemolymph nutrients.
An intriguing observation in insects is the synchronization of organ growth
and the developmental timing program. Growth perturbation and damage
to the imaginal disc delay pupariation, which allows extra time for tissues
to regenerate or grow (
Halme, Cheng, & Hariharan, 2010; Poodry &
Woods, 1990; Simpson, Berreur, & Berreur-Bonnenfant, 1980; Stieper,
Kupershtok, Driscoll, & Shingleton, 2008
). During the extended growth
period, non-affected discs reduce their growth rate to prevent overgrowth
in order to maintain their final size relationship with the damaged or
growth-perturbed discs (
Parker & Shingleton, 2011
). Discs therefore
sense growth perturbation and damage, and signal to other tissues to slow their
growth as well as to the neuroendocrine system to attenuate the production
of ecdysone and extent the growth period. The signal from damaged disc
may include a role for retinoids (
Halme et al., 2010
). However, recently
two independent studies demonstrated that growth-retarded discs secrete a
peptide exhibiting structural similarity with insulin, named
Drosophila
insulin-like peptide 8
(
DILP8
), that delays pupariation and suppresses systemic
growth (
Colombani et al., 2012; Garelli et al., 2012
). This peptide has a con-
served cysteine motif that is characteristic for members of the insulin-relaxin
peptide family.
DILP8
is strongly induced in discs when their growth is
retarded or if they are damaged, indicating that it might be a downstream signal
of the JNK pathway. Knock down of
DILP8
is sufficient to suppress the delay
of pupariation in larvae with damaged discs. Furthermore,
DILP8
over-
expression delays pupariation and also prevents overgrowth during the pro-
longed growth period (
Garellietal.,2012
). Overexpression of
DILP8
and
discs damage mostly prolong the duration of L3 (
Colombani et al., 2012;
Garelli et al., 2012
), like lack of PTTH signaling (
McBrayer et al., 2007;
Rewitz et al., 2009
). The effect of DILP8 on ecdysone synthesis may therefore
be mediated through its suppressive effects on PTTH-producing neurons as
well as on the level of the PG response (
Colombani et al., 2012; Garelli
et al., 2012
). DILP8 has no influence on patterning and morphology of the
discs, indicating that it acts downstream of a disc growth or a damage sensing
system but upstream of the neuroendocrine system (
Colombani et al., 2012
).
Moreover,
ex vivo
organ co-culture experiments demonstrate that DILP8 is a
secreted factor that suppresses ecdysone production of brains with the PG
attached (
Colombani et al., 2012
).
The discs growth program is therefore a checkpoint for activation of the
neuroendocrine system and for the general growth control of other tissues.
