Biology Reference
In-Depth Information
component in the PTTH signaling machinery or ecdysone biosynthetic
pathway. Interestingly, nutrient-dependent
torso
expression has been
observed in
Bombyx
(
Young, Yeh, & Gu, 2012
), perhaps involving insulin.
Moreover, the transcription factor Broad is required for expression of
torso
(
Xiang, Liu, & Huang, 2010
) and insulin induces expression of
broad
in the
wing disks of
Manduca
, overcoming the inhibition by JH (
Koyama,
Syropyatova, & Riddiford, 2008
). Assuming a similar scenario in the PG,
insulin might increase
broad
levels to upregulate
torso
expression, providing
competence to PTTH that in turn leads to commitment for metamorphosis.
In agreement with a role in regulating ecdysone synthesis,
broad
null mutants
fail to pupariate and
broad
is expressed in the PG after the L2/L3 transition
with a rapid increase during wandering as the ecdysone titer rises (
Kiss,
Beaton, Tardiff, Fristrom, & Fristrom, 1988; Zhou, Zhou, Truman, &
Riddiford, 2004
).
In the previous section, we considered how TOR in the fat body might
help generate FDSs that act either on the PG or PTTH activity. However
TOR signaling in the PG itself is also important for determining timing since
recent evidence suggests that TOR plays a role in the PG in the regulation of
ecdysone synthesis (
Layalle et al., 2008
). In contrast to moderate changes in
insulin signaling, reducing TOR activity in the PG prolongs larval develop-
ment after the critical weight checkpoint (
Colombani et al., 2005; Layalle
et al., 2008
). Although reducing TOR signaling delays pupariation, activa-
tion of TOR in the PG under normal food conditions does not accelerate
development (
Layalle et al., 2008
). This only occurs under conditions with
restricted nutrition, suggesting an upper limit for nutrient activation of
ecdysone signaling. Like TOR, increasing insulin signaling in the PG only
accelerates metamorphosis in larvae reared without yeast supplement (
Mirth
et al., 2005
). This again supports the idea that nutrients provide a positive
signal that is limited by the maximum growth rate. In contrast, increasing
Ras signaling in the PG dramatically accelerates metamorphosis even under
standard food conditions (
Rewitz, Yamanaka, et al. 2009
). The MAPK
pathway is the major pathway relaying the signal downstream of the PTTH
receptor Torso (
Fig. 1.3
). Like insulin signaling, activating the MAPK
pathway in the PG results in increased PG cell growth, and the larvae
pupariate at a smaller size than normal. On the other hand, decreasing
MAPK signaling in the PG results in developmental delay and overgrowth
similar to larvae lacking PTTH or Torso. Together with insulin, the impor-
tance of TOR signaling in the PG may help explain why overgrown larvae
lacking PTTH eventually pupariate (
McBrayer et al., 2007
).
