Data from: Stage-specific plasticity in ovary size is regulated by insulin/insulin-like growth factor and ecdysone signalling in Drosophila

Animals from flies to humans adjust their development in response to
environmental conditions through a series of developmental checkpoints,
which alter the sensitivity of organs to environmental perturbation.
Despite their importance, we know little about the molecular mechanisms
through which this change in sensitivity occurs. Here we identify two
phases of sensitivity to larval nutrition that contribute to plasticity in
ovariole number, an important determinant of fecundity, in Drosophila
melanogaster. These two phases of sensitivity are separated by the
developmental checkpoint called “critical weight”; poor nutrition has
greater effects on ovariole number in larvae before critical weight than
after. We find that this switch in sensitivity results from distinct
developmental processes. In precritical weight larvae, poor nutrition
delays the onset of terminal filament cell differentiation, the starting
point for ovariole development, and strongly suppresses the rate of
terminal filament addition and the rate of increase in ovary volume.
Conversely, in postcritical weight larvae, poor nutrition affects only the
rate of increase in ovary volume. Our results further indicate that two
hormonal pathways, the insulin/insulin-like growth factor and the
ecdysone-signaling pathways, modulate the timing and rates of all three
developmental processes. The change in sensitivity in the ovary results
from changes in the relative contribution of each pathway to the rates of
terminal filament addition and increase in ovary volume before and after
critical weight. Our work deepens our understanding of how hormones act to
modify the sensitivity of organs to environmental conditions, thereby
affecting their plasticity.