Biology Reference
In-Depth Information
This defines another concept important for attainment of final body size
which is the “terminal growth period” (also known as the interval to cessa-
tion of growth). The terminal growth period is the time interval between
attainment of critical weight and the cessation of feeding that occurs when
larvae transition to the wandering stage (
Edgar, 2006; Warren et al., 2006
).
It is important to note that after critical weight is achieved, development
proceeds on a fixed temporal schedule that is independent of nutritional
status. However, nutrients can still have a strong influence on final body size
during this time. If nutrient levels are high for instance, a normal body size is
produced, while if they are low a small adult is formed.
At least two size-related checkpoints, one mediated by growth and
energy status of the larval-specific tissues and the other mediated by the mat-
uration and patterning of adult precursor tissues, known as the imaginal
disks, regulate timing of metamorphosis (
Edgar, 2006; Poodry & Woods,
1990
). Starvation delays development in animals that lack imaginal disks,
suggesting that the mechanism which coordinates growth and ecdysone
release with the nutritional status resides in the nonmitotic larval cells.
2.2. Linking nutrition to developmental timing
Insects undergo a tremendous amount of growth from the embryo to the
final larval stage that is ready to initiate metamorphosis (
Britton & Edgar,
1998
). Because the environment affects growth rate, but not critical weight,
the larva must coordinate cellular growth and nutrient storage with the
timing of metamorphosis. Nutrients absorbed by the gut are not the only
signals that trigger cell growth in most organs. Instead, systemic growth
in
Drosophila
is regulated by seven insulin-like peptides known as Dilp1-7
that signal through a single conserved insulin receptor (InR) (
Rulifson,
Kim, & Nusse, 2002; Wu & Brown, 2006
). The insulin-producing cells
(IPCs) in the brain are major sites for Dilp production and release. However,
insulin signaling must be coordinated with nutrient availability which is
sensed by the fat body (analogous to adipose and liver tissues of vertebrates).
In a growth permissive, nutrient-rich environment, the fat body non-
cell-autonomously regulates growth through the release of fat body-derived
signals (FDSs) (
Colombani et al., 2003; Geminard, Rulifson, & Leopold,
2009; Rideout, Marshall, & Grewal, 2012
). In the fat body, TOR acts as
a sensor of nutrients from the gut and responds cell-autonomously to amino
acids and ATP levels. Amino acids are crucial dietary components for
growth and developmental progression. Although growth of some tissues
