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the onset of insect maturation that leads to the completion of all adult struc-
tures ( Fig. 1.1 A) ( Mizoguchi, 2001; Riddiford, Truman, Mirth, & Shen,
2010; Rountree & Bollenbacher, 1986 ). As one would expect, genetic
manipulations that cause (a) JH titers to prematurely regress, (b) interfere
with the expression of the JH receptor, and (c) mutations in enzymes
necessary for JH synthesis all trigger premature metamorphosis in a range
of insects ( Daimon et al., 2012; Gu & Tsai, 2012; Konopova & Jindra,
2007; Minakuchi, Namiki, Yoshiyama, & Shinoda, 2008; Tan, Tanaka,
Tamura, & Shiotsuki, 2005; Wang, Ali, Moriyama, Iwanaga, & Kawasaki,
2012 ). We will discuss the role of JH and developmental timing in a separate
section in further detail.
During insect development, pulses of ecdysone initiate all developmental
transitions, including the molts, wandering behavior, and metamorphosis.
Ecdysone is produced as a prohormone in the prothoracic glands, and fur-
ther processed in target tissues to achieve its biologically active form. Our
understanding of how the onset, amplitude, and duration of ecdysone pulses
are controlled is still incomplete. However, we do know that the rhythmic
release of PTTH, a brain-derived neuropeptide, elicits the onset of ecdysone
pulses ( Rybczynaki, 2005 ), similar to what was described for adrenocortico-
tropic hormone (ACTH) and glucocorticoids in vertebrates ( Lightman &
Conway-Campbell, 2010 ). PTTH transcripts display ultradian rhythmicity
in Drosophila ( McBrayer et al., 2007 ), which in turn is under control of brain
neurons that are critical for establishing circadian behaviors, and we will
explore this relationship in more detail in the next section.
To initiate a transition between two developmental stages, the brain
releases PTTH ( Fellner, Rybczynski, & Gilbert, 2005; Kawakami et al.,
1990; McBrayer et al., 2007; Westbrook & Bollenbacher, 1990 ), which
induces a signaling cascade that activates ecdysone biosynthesis in PG cells
( Gilbert, 2004; Rewitz, O'Connor, & Gilbert, 2007 ) and its secretion
into the hemolymph ( Huang, Warren, & Gilbert, 2008 ). Once ecdysone
reaches its target tissues, it is converted into its active form,
20-hydroxyecdysone (20E) and binds the heterodimer of two nuclear recep-
tors, ecdysone receptor (EcR) and ultraspiracle (USP) ( King-Jones &
Thummel, 2005; Koelle et al., 1991; Yao et al., 1993 ) resulting in the acti-
vation of a transcriptional response that drives behavioral and physiological
changes as well as the molts ( Bollenbacher, Agui, Granger, & Gilbert, 1979;
Bollenbacher, Smith, Goodman, & Gilbert, 1981; Jiang, Lamblin, Steller, &
Thummel, 2000; King-Jones & Thummel, 2005; Riddiford, 1993;
Sullivan & Thummel, 2003; Thummel, 1996, 2002 ). The nature of a molt
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