Biology Reference
In-Depth Information
tissue-autonomous program and provides a mechanism for how genetic pro-
grams determining organ size allows growth assessments by the developmental
timing system.
Despite the recent progress, some important questions remain: What are
the targets of DILP8 and how does this signal converge on ecdysone synthe-
sis? Identifying its receptor will help clarifying these issues. Although it is
possible that DILP8 acts antagonistically on InR, the fact that the disc check-
point can delay pupariation post critical weight (
Hackney et al., 2012
) sug-
gests otherwise, since timing is then independent of InR (
Shingleton et al.,
2005
). DILP8 is structurally related to the relaxin family and may act through
one of the
Drosophila
relaxin family receptors, Lgr3 and Lgr4, for which the
ligand and their function remain unknown (
Hauser et al., 2008; Van Hiel,
Vandersmissen, Van Loy, & Vanden, 2012
).
6. CONCLUSIONS AND PERSPECTIVES
In summary, developmental timing of maturation in
Drosophila
is con-
trolled by the endocrine system that makes assessments of nutrition and
growth status of the developing organism. This requires crosstalk between
the endocrine system and organs that communicate nutritional levels and
their growth status. Recent advances in
Drosophila
have shown that the over-
all architecture underlying timing of maturation is remarkably conserved and
has demonstrated that secreted insulin-like molecules establish an important
connection between nutrients, growth sensing, and the endocrine system.
Like inmammals, maturation in
Drosophila
is controlled by a neuroendocrine
axis that ultimately produces a steroid signal triggering developmental and
behavioral changes associated with this transition. The release of ecdysone
only occurs once the larva has passed certain checkpoints ensuring accumu-
lation of enough nutrients and completion of sufficient growth during
development to reach sexual maturity at a genetically determined final adult
size. Consistent with the overall conservation of the system, the insulin-like
molecules that are key to adjust the duration of juvenile development (the
developmental timer) to dietary conditions have been conserved during
evolution.
The recent identification of the secreted signal molecules Upd2 and
DILP8 has provided important new information, and also raised several
questions. Upd2 is functionally related to the human leptin which is linked
to obesity and is expressed in adipose tissue in response to fat and affects
timing of maturation, like
upd2
in
Drosophila
(
Roa et al., 2009
). Considering
