Biology Reference
In-Depth Information
Determining the precise temporal timing of Dilp8 activity and whether it
correlates with one of the other small ecdysone peaks is an important area for
future investigation. Interestingly, normal
Dilp8
expression peaks early dur-
ing the third instar and drops from 80 to 96 h AEL (after egg laying)
(
Colombani et al., 2012
). The drop in
Dilp8
expression coincides with
the time when larvae reach critical weight at about 80 h AEL. This may sug-
gest that the endocrine system is reading the Dilp8 drop as the critical weight
checkpoint is reached. However, disk damage mainly delays pupariation by
increasing the terminal growth period (
Stieper et al., 2008
), which indicates
that the disks exert their suppressive influence postcritical weight, whereas
nutritional restriction has no effect beyond this point. Moreover, tissue dam-
age in the imaginal disks 96 h AEL, well after passing the critical weight
checkpoint, delays pupariation (
Wells & Johnston, 2012
). Thus, maturation
of larval-specific and adult precursor tissues may not coincide, and critical
weight and imaginal disk maturation are likely different checkpoints, each
of which may independently regulate the small fluctuations in the ecdysone
titer prior to the larger molting peak. Although passing the critical weight
checkpoint leads to nutrient-independent patterning of the disks (
Mirth,
Truman, & Riddiford, 2009
), overexpression of
Dilp8
, which delays
pupariation, does not influence disk patterning (
Colombani et al., 2012
),
suggesting that
Dilp8
decrease is the result, and not the cause, of disk
maturation. The fact that
Dilp8
mutants pupariate almost on time further
supports the view that two independent timing mechanisms exist, one in
the adult progenitor tissues and one in the larval-specific tissues. A detailed
analysis of the exact time for the drop in
Dilp8
expression and the ecdysone
profile may help unraveling if Dilp8 is responsible for the critical weight
peak or one of the subsequent low-level ecdysone peaks. Taken together,
these data together with the fact that manipulating insulin signaling in the
disks does not affect timing (
Stieper et al., 2008
) show that ecdysone
production is controlled by a developmental checkpoint run by an intrinsic
genetic program that monitors disk maturation and patterning largely
independent of nutrients.
2.4. The brain relays internal and external cues
to the endocrine system
Some checkpoint signals from peripheral tissues such as fat body and disks are
likely communicated through the central brain to the endocrine system. For
example, nutritional assessment must ensure that shutdown of feeding only oc-
curs when enoughmass has been accumulated to survive the nonfeedingmeta-
morphic stage. The brain regulates insulin release from the IPCs in response to
