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conserved in
Drosophila
, suggesting that critical weight is determined
through another mechanism (
Nijhout, 2003; Stern & Emlen, 1999
).
Recent studies have elucidated some of the mechanisms required for
critical weight assessment in
Drosophila
. One study showed that the
Droso-
phila
insulin receptor (InR), which has a conserved role in nutrition-
dependent growth in animals, affects growth differently in precritical weight
and postcritical weight larvae (
Shingleton, Das, Vinicius, & Stern, 2005
).
Before larvae reach critical weight, InR signaling influences developmental
timing but not larval growth. In contrast, InR activity affects final body size
but not developmental timing in postcritical weight larvae. This is consistent
with the observations in starved larvae discussed above. Several other studies
showed that in
Drosophila
the size of the PG affects developmental rate and
body size (
Caldwell, Walkiewicz, & Stern, 2005; Colombani et al., 2005;
Mirth, Truman, & Riddiford, 2005
). They did this by manipulating
insulin-dependent growth in the PG. When PG growth was suppressed
by the expression of PTEN, a phosphatase that antagonizes class I PI3K ac-
tivity, dominant negative class I PI3K, or dominant negative Ras, the larvae
were larger than controls and had a longer developmental period. Con-
versely, larvae with an enlarged PG due to either class I PI3K or Ras acti-
vation initiated metamorphosis earlier than controls and thus the adults were
smaller. Interestingly, the effects of growth in the PG appear to be specific to
the insulin signaling pathway and not to cell size increase in general. In the
study done by Colombani et al., they increased PG size by manipulating two
other growth pathways in addition to PI3K: Myc and cyclin D/Cdk4.
Although activation of these two genes increased the size of the PG, they
had no effect on pupal or adult size (
Colombani et al., 2005
).
It is clear from these studies that tissue growth coordinates with devel-
opmental timing through InR signaling; however, the signals that regulate
this have not been well studied. Recently, two independent groups per-
formed screens to identify molecules that couple tissue growth with devel-
opmental timing and identified a novel
Drosophila
insulin-like peptide (dilp),
dilp8
(
Colombani, Andersen, & L
ยด
opold, 2012; Garelli, Gontijo, Miguela,
Caparros, & Dominguez, 2012
). Perturbing growth of larval imaginal disks
through either damage or tumor promotion causes a delay in the time to
pupariation, allowing the imaginal disks to reach their correct size
(
Menut et al., 2007; Poodry & Woods, 1990; Simpson, Berreur, &
Berreur-Bonnenfant, 1980; Smith-Bolton, Worley, Kanda, & Hariharan,
2009
).
dilp8
is highly induced in imaginal disks with growth perturbations
(
Colombani et al., 2012; Garelli et al., 2012
). Importantly, knockdown of
