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Fig. 8. Model depicting changing levels of growth activators and inhibitors
synthesized by disc cells in relation to increases in cell number. This model
is a variation of a model proposed by Nijhout to explain how rising levels of
growth inhibitors may determine disc size
(Nijhout, 2003). In Nijhout's
model, imaginal disc cells produce growth activators and inhibitors, and the
inhibitors sequester or inactivate the activators. The level of each factor
depends on the number of cells at the time and the influence of the inhibitor
over the activator. At first activator levels are high, inhibitor levels low
and disc growth is approximately exponential. When inhibitor levels become
sufficiently high, growth begins to slow. Nijhout's model proposes that
inhibitor activity remains high throughout slow growth. Accordingly, if
pixie mutant cells were sensitive to the presence of inhibitor, then
pixie mutant clone growth would be expected to worsen towards the end
of larval life and during metamorphosis as growth slows. Instead,
pixie mutant clone growth (survival) improves at the end of larval
life (see text and Fig. 6E,F),
and the intensity of cell death in pixie mutant and Minute
discs decreases shortly before pupation
(Fig. 4). Thus, we propose that
the presence of activator is necessary for inhibitor synthesis. When inhibitor
levels reach a threshold, this triggers the slowing down of growth and
inactivation of the activator, which in turn leads to downregulation of
inhibitor synthesis. Thus the pixie mutant clone phenotype is strong
at the beginning of the slow phase, when inhibitor levels are high, but weak
at the end of larval life when inhibitor levels are low, and growth is slow.
The graphs presented here potentially apply to both the hinge and the pouch,
with higher levels of inhibitors being found in the pouch than the hinge.
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