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unresponsive to methoprene and JH-III (
Konopova & Jindra, 2007;
Parthasarathy, Tan, & Palli, 2008
). In
Drosophila
, the removal of CA causes
the formation of smaller pupae and death at head eversion (
Riddiford,
Truman, Mirth, & Shen, 2010
), and the
Met
/
gce
double mutant dies during
the larval-pupal transition, although both
Met
and
gce
null single mutants are
viable because of their redundancy (
Abdou et al., 2011
).
Met protein specifically binds JH-III and other biologically active JH
mimics at physiologically relevant concentrations [
K
d
¼
5.3 nM for JH-III in
Drosophila
(
Miura, Oda, Makita, & Chinzei, 2005
);
K
d
2.94 nM for JH-III
in
Tribolium castaneum
(
Charles et al., 2011
)]. This binding is through the
C-terminal PAS-B domain (
K
d
¼
12.3 nM) (
Charles et al., 2011
). Met forms
Met/Met homodimers [also Met/GCE heterodimers in
Drosophila
(
Godlewski et al., 2006
)] in the absence of JH, and dimer formation was
prevented by JH (
Charles et al., 2011; Godlewski et al., 2006
). In themosquito,
A. aegypti
, a transcriptional coactivator of the ecdysteroid receptor complex
FISC (
Li, Mead, & Zhu, 2011
) and a steroid receptor coactivator SRC (also
known as Taiman) (
Zhang, Xu, Sheng, Sui, & Palli, 2011
), both of which
belong to the member of the bHLH-PAS family, act as functional partners
of Met in mediating JH action on target genes such as
Kru
¨
ppel-homolog
1
(Kr-h1). Unlike in the case of the Met/Met formation, Met/FISC and Met/
SRC form a complex in the presence of JH (
Charles et al., 2011; Li et al.,
2011
).Mutations of
Tribolium
Metwithin the ligand-bindingpocketwhichdis-
rupt JH binding did not affect the formation of the Met/Met dimer complex,
but prevented the ligand-dependent dissociation of the Met/Met homodimer
and the ligand-dependent interaction of Met with its partner SRC (Taiman)
(
Charles et al., 2011
). The evidence of both biological actions and the charac-
teristic nature of Met such as direct and specific binding to JH strongly suggest
that Met is a JH receptor with SRC (Taiman) as a partner (
Fig. 3.5
A).
¼
3.2. JH responsive genes and the JH signaling pathway
Kr-h1
is an evolutionarily conserved JH-induced gene that seems to be a
crucial factor for molting and metamorphosis in both holometabolous and
hemimetabolous insects (
Duportets et al., 2012, Lozano & Belles, 2011;
Minakuchi, Namiki, & Shinoda, 2009; Minakuchi, Zhou, & Riddiford,
2008; Zhu, Busche, & Zhang, 2010
). RNAi knockout of the
Kr
-
h1
gene
induces precocious metamorphosis in
Tribolium
(
Minakuchi et al., 2009
)
and
Blattella
(
Lozano & Belles, 2011
), but the JH analog methoprene was
unable to rescue this effect so that Kr-h1 is considered to mediate the JH
