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Tissue-specific regulation of juvenile hormone esterase gene expression by 20-hydroxyecdysone and juvenile hormone in Bombyx mori.

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Archives of Insect Biochemistry and Physiology 65:143–151 (2007)
Tissue-Specific Regulation of Juvenile Hormone
Esterase Gene Expression by 20-Hydroxyecdysone
and Juvenile Hormone in Bombyx mori
Manabu Kamimura,* Michiyoshi Takahashi, Kyoko Kikuchi, A.M.S. Reza, and
Makoto Kiuchi
Juvenile hormone esterase (JHE) is the primary juvenile hormone (JH) metabolic enzyme in insects and plays important roles
in the regulation of molt and metamorphosis. We investigated its mRNA expression profiles and hormonal control in Bombyx
mori larvae. JHE mRNA was expressed at the end of the 4th and 5th (last) larval instars in the midgut and in all the three
(anterior, middle, posterior) parts of the silk gland. In the fat body, JHE expression peaked twice in the 5th instar, at wandering and before pupation, while it gradually decreased through the 4th instar. When 20-hydroxyecdysone (20E) was injected
into mid-5th instar larvae, JHE mRNA expression was induced in the anterior silk gland but suppressed in the fat body. Topical
application of a juvenile hormone analog fenoxycarb to early-5th instar larvae induced JHE expression in both tissues. In the
anterior silk gland, JHE expression was accelerated and strengthened by 20E plus fenoxycarb treatments compared with 20E or
fenoxycarb single treatment, indicating positive interaction of 20E and JH. JHE mRNA is thus expressed in tissue-specific
manners under the control of ecdysteroids and JH. Arch. Insect Biochem. Physiol. 65:143–151, 2007. © 2007 Wiley-Liss, Inc.
KEYWORDS: juvenile hormone; esterase; ecdysone; Bombyx mori; silkworm; silk gland; fat body
INTRODUCTION
In insect, molt and metamorphosis are orchestrated by ecdysteroids and juvenile hormone (JH).
Ecdysteroids, primarily 20-hydroxyecdysone (20E),
initiate molting and JH determines the molt characteristics: pulses of 20E in the presence of JH trigger larval-larval molts, and in its absence cause a
larval-pupal molt followed by pupal-adult transformation (Riddiford, 1985). Hemolymph JH titer is controlled by synthesis in the corpora allata
and degradation in hemolymph and other periph-
eral tissues (Hammock, 1985). The primary route
of JH degradation is hydrolysis of its methyl ester
by the highly specific JH esterase (JHE). Another
route of JH degradation is hydration of the 10,11epoxide by JH epoxide hydrolase. The importance
of JHE in the metabolism of JH, control of hemolymph JH titer, and induction of metamorphosis
has been demonstrated by enzymatic inhibition
using transition state analogue inhibitors (AbdelAal and Hammock, 1990; Browder et al., 2001)
and molecular genetic manipulation of JHE gene
expression using baculovirus expression systems or
National Institute of Agrobiological Sciences, Tsukuba, Ibaraki, Japan
Contract grant sponsor: Ministry of Agriculture, Forestry and Fisheries of Japan; Contract grant sponsor: Bio-oriented Technology Research Advancement Institution
(PROBRAIN) of Japan.
A.M.S. Reza’s present address is Department of Zoology, Rajshahi University, Rajshahi-6205, Bangladesh.
*Correspondence to: M. Kamimura, Invertebrate Gene Function Research Unit, National Institute of Agrobiological Sciences, 1-2 Owashi, Tsukuba, Ibaraki
305-8634, Japan. E-mail: kamimura@affrc.go.jp
© 2007 Wiley-Liss, Inc.
DOI: 10.1002/arch.20186
Published online in Wiley InterScience (www.interscience.wiley.com)
144
Kamimura et al.
transgenic insects (Bonning et al., 1997; Hajos et
al., 1999; Tan et al., 2005). In the silkworm Bombyx
mori, JHE is mainly synthesized in the fat body and
secreted into the hemolymph in the last larval instar, where it degrades remaining JH and potentiates the larval-pupal transition (Hirai et al. 2002).
JHE expression is induced by JH in several insects (Feng et al., 1999; Kethidi et al., 2005; Venkataraman et al., 1994; Vermunt et al., 1999;
Wroblewski et al., 1990). In the spruce budworm
Choristoneura fumiferana (Feng et al. 1999) and
in D. melanogaster (Kethidi et al., 2005), 20E suppresses JH-induced JHE expression. In a previous
study, we reported that feeding 20E in the early5th instar suppressed the increase of JHE activity
in hemolymph and application of an imidazole
compound KK-42, which blocks ecdysone synthesis in the prothoracic gland and causes a precocious metamorphosis, in the 4th instar induced
JHE mRNA expression in the fat body and the
appearance of JHE activity in hemolymph (Hirai
et al., 2002). Thus, it appears that JH expression
is also hormonally controlled in the silkworm;
however, the regulatory mechanisms involved are
still mostly unknown.
In the course of a screen to identify ecdysteroidregulated genes from the Bombyx anterior silk gland
by mRNA differential display (Kamimura et al.,
1999), we have identified JHE as an ecdysteroidinducible gene independently of the JHE expression study mentioned above. A 1.1-kbp RT-PCR
fragment encoding a part of the cloned JHE cDNA
(942-2035; Hirai et al., 2002) was strongly amplified from the anterior silk gland treated with JH
plus 20E and weakly amplified from those treated
only with 20E but not amplified from the control.
These results suggested that JHE mRNA expression
was positively regulated both by 20E and JH in
the Bombyx anterior silk gland. So far, there has
been no report showing that 20E can induce JHE
expression in any insect species. To clarify this
point, we investigated temporal expression profiles
and hormonal regulation of JHE and mRNA in
multiple tissues. The results suggest that the different responses to the hemolymph ecdysteroid titer yield tissue-specific JHE expression profiles.
MATERIALS AND METHODS
Insects and Hormonal Treatment
F1 hybrid silkworms, strain C145 × N140, were
reared on an artificial diet (Silkmate, Nihon Nosan
Kogyo, Yokohama, Japan) under a 12-h light:dark
photoperiod at 25 ± 1°C. The penultimate (4th)
instar was staged at the onset of the scotophase
and last (5th) instar at the photophase. Only female-determined larvae were used for experiments.
Fifty micrograms of 20-hydroxyecdysone (20E;
Sigma, St. Louis, MO) dissolved in 20 µl of distilled
water were injected into the silkworm through the
first abdominal leg with a microsyringe. One or 100
ng of a JH analog, fenoxycarb, supplied by Sankyo
Corporation (Tokyo, Japan), were dissolved in 5 µl
acetone and applied topically to the silkworm with
a micropipet along the dorsal midline. Physiological responses of silkworms to those hormonal treatments were described in Kamimura and Kiuchi
(1998) and Takahashi et al. (2003) in detail.
Northern Blot Hybridization and
Quantitative RT-PCR
Total RNA was extracted by the acid guanidinium-phenol-chloroform method using TRIzol
(Gibco BRL, Rockville, MD). Twenty micrograms
of each RNA sample was separated on a guanidine
thiocyanate 1% agarose gel (Goda and Minton,
1995) and transferred to a Hybond NX nylon membrane (Amersham Pharmacia Biotech, Uppsala,
Sweden). Membranes were hybridized with DNA
probes labeled with alpha [α-32P]-dATP using a
Strip-EZ™ DNA kit (Ambion, Austin, TX). A 1.1kbp PCR fragment encoding a part of the JHE
cDNA (942-2035; GenBank No. AF287267) was
used as a probe for JHE. Hybridization, washing,
and stripping of blots were based on the manufacturer’s instructions. Signals were detected using
an image analyzer (Molecular Imager GS-250, BioRad, Hercules, CA).
Five micrograms of total RNA were reverse-transcribed with an oligo (dT) primer using Ready-ToGo You-Prime First-Strand Beads (Amersham PharArchives of Insect Biochemistry and Physiology
July 2007
doi: 10.1002/arch.
Hormonal Regulation of Silkworm JHE
macia Biotech, Uppsala, Sweden) and used for
quantitative PCR on a real-time thermal cycler
(model 7700, Applied Biosystems). Serial dilutions
of a pBluescript II plasmid containing the full coding region of JHE cDNA were used as standards. A
fluorogenic TaqMan probe JHE-pro1 5′-TGCCGA
GAGTGAAACGATTGAGCAGG-3′. forward primer
JHE-51 5′-CACATGACGATCACGACCACT-3′, and
reverse primer JHE-31 5′-CCGTGATGTTGTCCA
CTCTCTTT-3′ were designed in the 3′ UTR. A ribosomal protein gene rp49 (GenBank: AB048205)
was chosen as a reference gene. A TaqMan probe
rp49-pro1 5′-TGGTTACGGTTCCAACAAGAAGAC
CCG-3′, forward primer rp49-51 5′-GGTCAATAC
TTGATGCCCAACA-3′, and reverse primer rp49-31
5′-GGAATCCATTTGGGAGCATATG-3′ were used as
in a previous report (Reza et al., 2004). PCR condition was based on the standard procedure on
the manufacturer’s instructions. The molar
amounts of JHE and rp49 cDNAs were calculated
on the basis of a crossing point analysis, with standard curves generated from the standard plasmids.
JHE cDNA amounts were normalized with rp49
cDNA amounts in the same samples.
Independent sets of RNA were used for northern blot analysis and quantitative RT-PCR.
145
gradually decreased through the instar (Fig. 1). In
the 5th instar, JHE mRNA expression had doublepeaked at wandering and just before pupation. This
expression profile is consistent with a previous report (Hirai et al., 2002). JHE mRNA expression in
the wing disc in the 5th larval instar was similar
to that in the fat body, except that overall expression levels were much lower (Fig. 1).
Developmental Regulation of JHE mRNA in the
Anterior Silk Gland
Detailed Northern blot analysis showed that
JHE mRNA was expressed strongly on day 3.0 in
the 4th larval instar and from day 10.0 to 11.0 in
the 5th larval instar in the anterior silk gland (Fig.
2). The JHE expression periods coincided with the
hemolymph ecdysteroid peaks. Trace amounts of
JHE mRNA could be detected in the early 4th instar but not in the 5th instar, indicating that the
basal JHE expression level is higher in the 4th instar than in the 5th larval instar. Quantitative RTPCR analysis showed a very similar JHE mRNA
expression profile (Fig. 2).
Hormonal Regulation of JHE mRNA in the
Anterior Silk Gland
RESULTS
Developmental Regulation of
JHE mRNA in Six Tissues
In the anterior silk gland, a trace level of JHE
mRNA was detected by Northern blot during the
first 3 days of the 4th larval instar (Fig. 1). Its expression increased on day 3 and then decreased to
the basal level on the next day. In the 5th larval
instar, JHE mRNA was detected only on day 10,
just before pupation. Very similar profiles of JHE
mRNA expression were observed in the middle and
posterior silk glands (Fig. 1). In the mid gut, strong
JHE expression was also observed before each molting, although it peaked not on day 3 but on day 4
in the 4th instar (Fig. 1).
In the fat body, JHE mRNA was expressed
strongly at the beginning of the 4th instar and
Archives of Insect Biochemistry and Physiology
July 2007
doi: 10.1002/arch.
When 20E was injected into the last instar larvae of day 4, JHE mRNA appeared 12 h post injection (p.i.) and was expressed most strongly 24 h
p.i. (Fig. 3A). Topical application of 100 ng fenoxycarb just after the 20E injection strengthened
and accelerated JHE mRNA: JHE mRNA expression
was induced 2 h p.i. and peaked 12 h p.i. (Fig.
3A). Application of fenoxycarb only also induced
JHE expression within 2 h (Fig. 3B). JHE mRNA
gradually increased until 36 h and remained at least
until 48 h after the application. The maximum level
of JHE expression after fenoxycarb treatment was
lower than after 20E alone or 20E plus fenoxycarb
treatments (data not shown). In the control larvae, JHE mRNA was undetectable throughout the
analyzed period (from day 4.0 to 6.0 of the 5th
instar: Fig. 2).
We topically applied 1 ng of fenoxycarb to the
146
Kamimura et al.
Fig. 1. Tissue-specific expression
profiles of JHE mRNA in the 4th
and 5th larval instar of the silkworm as detected by Northern
blot analysis. Ethidium bromide
staining of rRNA is shown as a
control for equal loading of RNA
samples.
last instar larvae on day 4 and analyzed JHE mRNA
expression in one- or two-day intervals (Fig. 3C).
This treatment induced a supernumerary molt into
an abnormal 6th instar larvae with evaginated pupal antennae and often with evaginated wings
(Kamimura and Kiuchi, 1998). JHE mRNA expression was induced immediately but transiently. JHE
mRNA would then reappear on day 11. The tim-
ing of the second JHE expression coincided with
the hemolymph ecdysteroid peak.
Topical application of 1 ng of fenoxycarb on
day 0 of the last instar larvae delayed the larvalpupal metamorphosis by 6 days (Kamimura and
Kiuchi, 1998). This JH treatment also induced JHE
mRNA expression at two different times, 2 days
after the application and just before pupation (Fig.
Archives of Insect Biochemistry and Physiology
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doi: 10.1002/arch.
Hormonal Regulation of Silkworm JHE
147
Fig. 2. Temporal expression profiles of JHE mRNA in the
anterior silk gland. In quantitative RT-PCR analysis
(middle panel), quantities of JHE cDNA in cDNA pools
were normalized to those of internal standard gene rp49.
Bars represent SE (N = 2). In Northern blotting analysis
(bottom panel), ethidium bromide staining of rRNA is
shown as a control for equal loading of RNA samples.
Hemolymph ecdysteroid and JH titers (top panel) are
based on Kiuchi (1992) and Niimi and Sakurai (1997),
respectively.
3D). The timing of the second JHE expression also
coincided with the hemolymph ecdysteroid peak.
larvae on day 4 suppressed JHE mRNA expression
(Fig. 4B). JHE mRNA disappeared 12 h p.i., while
JHE expression was approximately constant in water-injected control larvae.
Hormonal Regulation of JHE mRNA in the Fat Body
We also investigated the effects of hormonal
treatments on JHE mRNA expression in the fat
body, which showed a distinct JHE expression profile compared to that in the anterior silk gland (Fig.
1). When only acetone was applied to the last instar larvae on day 0, JHE mRNA started increasing
gradually from day 4 in the fat body (Fig. 4A) in
the same fashion as when no hormone was applied (Fig. 1). Topical application of 100 ng
fenoxycarb enhanced this JHE mRNA expression:
JHE mRNA was expressed earlier and more strongly
than in the control (Fig. 4A).
In contrast, injection of 20E into the last instar
Archives of Insect Biochemistry and Physiology
July 2007
doi: 10.1002/arch.
DISCUSSION
Northern blot and quantitative RT-PCR analyses showed that the timing of the maximum JHE
expression in the anterior silk gland coincides with
the peak of hemolymph ecdysteroid titer in both
the 4th and 5th larval instar (Fig. 2), as in the case
of some ecdysteroid-inducible genes, such as
chitinase (Takahashi et al., 2002), chitinase-related
gene 1 (Takahashi et al., 2002), and a nuclear receptor BHR3 (unpublished data). 20E injection
into the mid-5th instar larvae induced JHE expression (Fig. 3A). In addition, JHE mRNA was ex-
148
Kamimura et al.
Fig. 3. Effects of 20E and fenoxycarb treatments on JHE
mRNA expression in the anterior silk gland. A: Northern
blot analysis of JHE expression in last instar larvae of day
4 that were injected with 50 µg of 20E (+20E), injected
with 20E and topically applied with 100 ng of a JH analog fenoxycarb (+20E+JH). Ethidium bromide staining of
rRNA is shown as a control for equal loading of RNA
samples. B: Quantitative RT-PCR analysis of JHE expression in last instar larvae of day 4 that were topically applied with 100 ng of fenoxycarb. Quantities of JHE cDNA
in cDNA pools were normalized to those of internal standard gene rp49. Values followed by the same lowercase
letters do not differ significantly in statistical analysis (P
< 0.05, Tukey-Kramer test after logarithmic transformation). Bars represent SE (N = 2–3). C: Northern blot analysis (bottom) of JHE expression in last instar larvae of day
4 that were topically applied with 1 ng of fenoxycarb.
Hemolymph ecdysteroid titers (top) are based on Kamimura and Kiuchi (1998). D: Northern blot analysis (bottom) of JHE expression in last instar larvae of day 0 that
were topically applied with 1 ng of fenoxycarb. Hemolymph ecdysteroid titers (top) are based on Kamimura and
Kiuchi (1998).
pressed at the hemolymph ecdysteroid peak in two
types of fenoxycarb-applied larvae in which a supernumerary larval molt was induced (Fig. 3C) or
the last larval period was prolonged (Fig. 3D).
These results strongly indicate that high JHE expression at each molt is induced by the hemolymph ecdysteroid surge. Because JHE mRNA was
expressed a few days later than those of the ecdysone receptors A and B1 isoforms (Kamimura et al.,
1997) and early ecdysteroid-inducible genes, such
as Broad-complex (Reza et al. 2004) and E75A (unpublished data) in the 5th larval instar, induction
of JHE mRNA by 20E is indirect, probably depending on early ecdysteroid-inducible gene products.
Fenoxycarb application also induced JHE
mRNA expression in the anterior silk gland (Fig.
3B–D). The Bombyx JHE is, thus, a JH-inducible
gene like the JHE gene of several other insects
(Feng et al., 1999; Kethidi et al., 2005; Venkataraman et al., 1994; Vermunt et al., 1999;
Wroblewski et al., 1990). This induction was rapid
(within 2 h), suggesting that the transcription is
directly induced by JH via a putative JH response
element in the promoter region as is the ChoristoArchives of Insect Biochemistry and Physiology
July 2007
doi: 10.1002/arch.
Hormonal Regulation of Silkworm JHE
Fig. 4. Effects of 20E and fenoxycarb treatments on JHE
mRNA expression in the fat body as detected by Northern blot analysis. Last instar larvae of day 4 were injected
with 50 µg of 20E (A) or last instar larvae of day 0 were
topically applied with 100 ng of fenoxycarb (B). Ethidium
bromide staining of rRNA is shown as a control for equal
loading of RNA samples.
neura fumiferana JHE gene (Feng et al., 1999;
Kethidi et al., 2004). We surmise that induction of
JHE mRNA by fenoxycarb reflects the positive regulation of basal JHE expression by the hemolymph
JH titer. Basal JHE mRNA expression levels in the
4th instar was higher than in the 5th instar (Fig.
2), supporting this hypothesis. Taken all together,
we gather that hemolymph JH titer controls the
basal expression level of JHE and ecdysteroid surges
induce its high expression at molting in the anterior silk gland. JHE expression is probably regulated in similar manners in the remaining parts of
silk glands and the mid gut, because the JHE
mRNA expression profiles in these tissues were
similar to that in the anterior silk gland.
20E and JH positively interact in regulating JHE
expression in the anterior silk gland, because JHE
expression was accelerated and strengthened after
Archives of Insect Biochemistry and Physiology
July 2007
doi: 10.1002/arch.
149
a combined 20E plus fenoxycarb treatment compared to 20E or fenoxycarb single treatment (Fig.
3A,B). In C. fumiferana and Drosophila melanogaster,
20E reversely suppressed JH-induced JHE expression (Feng et al., 1999; Kethidi et al., 2005). In C.
fumiferana, 20E suppressed JH-induced binding of
nuclear proteins to JHRE (Kethidi et al., 2004). 20E
might act on putative JHRE also in the silkworm
JHE. JHE expression was not induced by the
ecdysteroid surge of the last larval instar in the C.
fumiferana mid gut (Feng et al. 1999), in contrast
to what we have observed in the B. mori mid gut
(Fig. 1). These results suggest that the response of
JHE to 20E is species-specific.
Developmental JHE mRNA expression profile
in the fat body was much different from that in
the anterior silk gland, suggesting that its hormonal
regulation is different between these two tissues.
Indeed, 20E injection suppressed JHE expression
in the fat body on day 4 of the 5th instar (Fig.
4B), although the same treatment induced it in the
anterior silk gland (Fig. 3A). This result suggests
that the rising titer of hemolymph ecdysteroid suppresses JHE expression in the fat body from day 7
to 8 of the 5th larval instar (Fig.1). However, JHE
mRNA increases again in the 5th instar just before
pupation in the fat body. This second JHE peak of
expression might be the result of upregulation by
the high ecdysteroid titer as in the anterior silk
gland at the same time. We surmise that the JHE
expression was directly downregulated by a small
rise of ecdysteroids (20–100 ng/ml) on day 7–8
and then indirectly upregulated by the same hormone at its peak (ca. 1,500 ng/ml) via ecdysteroidinduced transcriptional factors.
What is the biological significance of the high
JHE mRNA expression at each molt in the silk
gland and mid gut? We do not have enough evidence at this time to give a clear answer to this
question. What we can say is that the translated
JHE proteins in these tissues at the end of the 4th
instar are probably not secreted into the hemocoel
because neither JHE proteins nor JHE activities
were detected in hemolymph throughout the 4th
instar (Hirai et al., 2002). One possibility is that
JHE proteins expressed at that time are retained in
150
Kamimura et al.
the cytoplasm, the plasma membrane, or in the
extracellular matrix and degrade JH in or around
cells. At the larval stage, the primary function of
JH is to modify ecdysteroid activity and to determine the molt characteristics (Riddiford, 1985).
JHE expression during molting may enable the tissues to degrade the remaining JH in or around tissues and prepare to respond to hemolymph JH in
the next instars. This hypothesis will be verified by
examining JHE activity and JHE protein expression
in these tissues.
ACKNOWLEDGEMTS
We thank Dr. Yasushi Kanamori with the assistance of quantitative RT-PCR. We also thank Dr.
Takahiro Shiotsuki and Dr. Yuichi Nakahara for
valuable discussion. This work was supported in
part by a Grant-in-Aid (Bio Design Program) from
the Ministry of Agriculture, Forestry and Fisheries
of Japan and by the Program for Promotion of Basic Research Activities for Innovative Biosciences
(PROBRAIN).
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