Biology Reference
In-Depth Information
(
Rybczynski, 2005
). Studies in
Manduca
and
Bombyx
have shown that the
PTTH prohormone is synthesized in a pair of neurosecretory cells in the
brain, and released into the hemolymph, where it is processed into its mature
form before it reaches the prothoracic glands (
Kawakami et al., 1990;
Westbrook & Bollenbacher, 1990
). In contrast,
Drosophila
PTTH-
producing neurons innervate the prothoracic gland directly, resulting in
the release of PTTH in the immediate vicinity of prothoracic gland cells
(
Fig. 2.4
A). The gene encoding
Drosophila
PTTH was only recently iden-
tified, which opened the door to genetically dissecting the PTTH signaling
pathway. Unfortunately, no mutants for the
Drosophila ptth
gene currently
exist; however, genetic ablation of PTTH-producing neurons provided
valuable insights into this signaling pathway (
McBrayer et al., 2007
). Surpris-
ingly, removing PTTH function through ablation is not lethal to the animal;
rather, it results in prolonged larval stages and significantly larger animals
compared to controls. Remarkably, not all larval stages are equally delayed,
and it appears that larvae without functional PTTH reach the third instar
with comparatively small delays but then remain in this stage considerably
longer than the normal 2 days. PTTH-ablation does lower the expression
of the Halloween genes, especially
disembodied
and
phantom
, suggesting that
the developmental delay in these animals is caused by a reduced rate of ec-
dysone biosynthesis (
McBrayer et al., 2007
). The fact that loss-of-PTTH
function hardly results in delays of the first and second instars indicates that
ecdysone production occurs efficiently enough at these stages, even without
PTTH stimulation. This is interesting for several reasons: First, it seems to
suggest that PTTH acts as a booster of the Halloween genes transcription
toward the end of the third instar when ecdysone titers rise dramatically,
but that the previous molts do not require such a stimulus. This then raises
two questions: How are the previous molts temporally regulated in the ab-
sence of PTTH? Are Halloween transcripts expressed at high levels through-
out larval development, even without PTTH stimulation? A recent study
published from our lab agrees with this notion, based on the finding that ring
gland-specific microarrays show very high transcript levels of the classic Hal-
loween genes in the early third instar, long before PTTH stimulates the late
third instar peak (
Ou et al., 2011
).
How is the PTTH signal transduced in prothoracic gland cells? A recent
study identified a receptor for
Drosophila
PTTH, a receptor tyrosine kinase
called Torso, and showed that it activates a MAP kinase pathway (
Rewitz,
Yamanaka, Gilbert, & O'Connor, 2009
). In particular, upon binding
to PTTH, Torso activates a small GTPase, Ras, which in turn triggers
