The Questions of Developmental Biology

central region producing the Wingless protein. Evidence for this latter model comes from
Ramírez-Weber and Kornberg (1999), who identified extremely thin processes extending from
the peripheral cells, across the wing disc, to the sites of Wingless synthesis (Figure 18.20).
These actin-based extensions are called cytonemes, and they are similar to the thin filopodia of
sea urchin mesenchymal cells. Evidence
has yet to show that they are active in
transporting the Wingless protein to the
peripheral cells. However, this is an
exciting and unexpected mechanism for
some types of long-range cell-cell
communication.
Proximal-distal axis: wingless protein
In addition to acting as a morphogen defining the dorsal-ventral axis, the Wingless protein also
acts to promote cell division and the extension of the wing (Neumann and Cohen 1996). The
interaction between the dorsal-ventral and anterior-posterior axes at their boundaries is critical for
the outgrowth along the proximal-distal axis. During metamorphosis, the "distalization" of the
proximal-distal axis from the base of the thorax outward to the tip of the wing or leg is
accomplished by cell interactions at the boundaries between the other two axes.*
Hormonal control of insect metamorphosis
Although the detailed mechanisms of insect metamorphosis differ among species, the
general pattern of hormone action is very similar. Like amphibian metamorphosis, the
metamorphosis of insects appears to be regulated by effector hormones, which are controlled by
neurohormones in the brain (for reviews, see Gilbert and Goodman 1981; Riddiford 1996). Insect
molting and metamorphosis are controlled by two effector hormones: the steroid 20-
hydroxyecdysone and the lipid juvenile hormone (JH) (Figure 18.21). 20-hydroxyecdysone
initiates and coordinates each molt and regulates the changes in gene expression that occur during
metamorphosis. Juvenile hormone prevents the ecdysone-induced changes in gene expression that
are necessary for metamorphosis.
Thus, its presence during a molt ensures that the result of that molt produces another
instar, not a pupa or an adult. The molting process is initiated in the brain, where neurosecretory
cells release prothoracicotropic hormone (PTTH) in response to neural, hormonal, or
environmental signals. PTTH is a peptide hormone with a molecular weight of approximately
40,000, and it stimulates the production of ecdysone by the prothoracic gland. This ecdysone is
modified in peripheral tissues to become the active molting hormone 20-hydroxyecdysone. Each
molt is initiated by one or more pulses of 20-hydroxyecdysone. For a larval molt, the first pulse
produces a small rise in the hydroxyecdysone concentration in the larval hemolymph (blood) and
elicits a change in cellular commitment.
A second, large pulse of hydroxyecdysone initiates the differentiation events associated
with molting. The hydroxyecdysone produced by these pulses commits and stimulates the
epidermal cells to synthesize enzymes that digest and recycle the components of the cuticle.