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are functionally redundant JH receptors in
Drosophila
.
Gce
and
Met
are rep-
resented by a single gene outside the
drosophilid
branch, due to a recent gene
duplication in this lineage.
While there is little doubt that Gce/Met function as the principal JH
receptors in
Drosophila
, the phenotypes that are usually associated with JH
deficiency in other insects, such as precocious development or a decreased
number of larval instars, are largely absent in
Drosophila gce
/
Met
double
mutants, suggesting that the role of
Drosophila
JH deviates from most other
insects (
Baumann, Fujiwara, & Wilson, 2010
). Despite this,
gce
/
Met
double
mutants displayed precocious induction of the
broad
gene, a key player in the
ecdysone-induced gene hierarchy controlling the larval-prepupal transition
(
Abdou et al., 2011
). This precocious induction is caused by the loss of
kruppel-homolog-1
(
kr-h1
) expression, which encodes a JH-inducible tran-
scription factor (
Minakuchi, Namiki, & Shinoda, 2009; Minakuchi,
Zhou, & Riddiford, 2008; Zhu, Busche, & Zhang, 2010
) that is normally
expressed during larval stages, but then sharply turned off in mid-prepupae
to allow for the upregulation of
broad
(
Pecasse, Beck, Ruiz, & Richards,
2000
). A recent study identified a functional JH-response-element
2kb
upstream of the
Bombyx kr-h1
gene, to which Met2, one of the two Met
orthologs found in
Bombyx
, was able to bind to when co-expressed with
another bHLH-PAS protein, SRC (
Kayukawa et al., 2012
). A similar JH
response element was also identified in the
kr-h1
gene from
Aedes aegypti
(
Shin, Zou, Saha, & Raikhel, 2012
). These data strongly suggest that
Kr-h1 is a key mediator of juvenile stages, and that precocious absence
of this factor initiates developmental programs that normally occur much
later. Finally,
gce
/
Met
double mutants exhibited precocious induction of
programmed cell death of larval fat body cells, a phenotype that is also con-
sistent with reduced JH signaling. Taken together, when JH receptor func-
tion is abolished in
Drosophila
, phenotypes are not nearly as dramatic as
expected, but still consistent with JH mediating juvenile stages in this
species.
Both, the redundancy of the
Drosophila
Gce and Met receptors and the
subtle defects on developmental timing limit the usefulness of
Drosophila
as a
model for studying JH and Met function. Recently, investigators focused
their attention to the red flour beetle
Tribolium castaneum
to study JH path-
ways. Disrupting
Met
function in
Tribolium
via RNAi not only caused resis-
tance to topical application of JH, but—in stark contrast to
Drosophila
—also
caused early larval stages to enter precocious metamorphosis, which pro-
vided strong genetic evidence that Met might be the long-sought-after
JH receptor (
Konopova & Jindra, 2007
). In addition, the authors observed
