Arthropod nuclear receptors and their role in molting

Nakagawa, Yoshiaki; Henrich, Vincent C.

doi:10.1111/j.1742-4658.2009.07347.x

Cited by 225 publications

(174 citation statements)

References 304 publications

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“…2), which is in agreement with the function domains for EcR (Bortolin et al 2011). In insects, differences among EcR isoforms mainly exist in the A/B domain caused by alternative splicing, and their expressions are regulated by different promoters (Nakagawa & Henrich 2009, Watanabe et al 2010. Unlike in insects, all three SpEcR isoforms from S. paramamosain had a same A/B domain, indicating that they were probably transcribed under the regulation of a same promoter.…”

Section: Discussionsupporting

confidence: 77%

Ecdysone receptor in the mud crab Scylla paramamosain: a possible role in promoting ovarian development

Gong¹,

Ye²,

Xie³

et al. 2015

Journal of Endocrinology

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In arthropods, it is known that ecdysteroids regulate molting, limb regeneration, and reproduction through activation of the ecdysone receptor (EcR). However, the ecdysteroid signaling pathway for promotion of ovarian development in crustaceans is still unclear. In this study, three cDNA isoforms of EcR were cloned from the mud crab Scylla paramamosain. qRT-PCR revealed that the SpEcR mRNA was abundant in the eyestalk, ovary and epidermis. During ovarian development, the SpEcR transcripts increased from stage I (undeveloped stage) and reached a peak at stage IV (late vitellogenic stage) before dropping to a lower level at stage V (mature stage). Meanwhile, levels of 20-hydroxyecdysone (20E) in the hemolymph, detected by HPLC-MS, displayed a similar pattern of increase with ovarian development. Results from in situ hybridization indicated that SpEcR mRNA was present in the follicular cells during vitellogenesis. Results from in vivo experiments revealed that 20E at 0.2 mg/g body weight significantly stimulated the expression of SpEcR and vitellogenin (SpVg) in female crabs during the early vitellogenic stage but not during the previtellogenic stage. This was confirmed by results from in vitro experiments which indicated that SpEcR and SpVg expression levels were significantly upregulated in early vitellogenic ovarian explants incubated with 5.0 mM 20E at 3 and 6 h but not in previtellogenic ovarian explants. Finally, results from in vitro gene silencing experiments indicated that the expression of SpEcR and SpVg in the ovary was significantly inhibited by SpEcR dsRNA. All these results together indicated that in S. paramamosain, 20E, and SpEcR, located in the follicular cells, play important roles in the promotion of ovarian development via regulating the expression of SpVg.

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Section: Discussionsupporting

confidence: 77%

Ecdysone receptor in the mud crab Scylla paramamosain: a possible role in promoting ovarian development

Gong¹,

Ye²,

Xie³

et al. 2015

Journal of Endocrinology

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“…For controlling metamorphosis, JH works in close cooperation with molting hormone (ecdysteroids) to prevent larvae from precociously turning into adults (status quo action). Although the mode of action of ecdysteroids in metamorphosis is well understood at the molecular level (4,5), that of JH is largely unknown (6).…”

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confidence: 99%

Transcriptional regulation of juvenile hormone-mediated induction of Krüppel homolog 1, a repressor of insect metamorphosis

Kayukawa

Minakuchi²,

Namiki³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

280

310

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The Krüppel homolog 1 gene (Kr-h1) has been proposed to play a key role in the repression of insect metamorphosis. Kr-h1 is assumed to be induced by juvenile hormone (JH) via a JH receptor, methoprene-tolerant (Met), but the mechanism of induction is unclear. To elucidate the molecular mechanism of Kr-h1 induction, we first cloned cDNAs encoding Kr-h1 (BmKr-h1) and Met (BmMet1 and BmMet2) homologs from Bombyx mori. In a B. mori cell line, BmKrh1 was rapidly induced by subnanomolar levels of natural JHs. Reporter assays identified a JH response element (kJHRE), comprising 141 nucleotides, located ∼2 kb upstream from the BmKr-h1 transcription start site. The core region of kJHRE (GGCCTCCACGTG) contains a canonical E-box sequence to which Met, a basic helix-loophelix Per-ARNT-Sim (bHLH-PAS) transcription factor, is likely to bind. In mammalian HEK293 cells, which lack an intrinsic JH receptor, ectopic expression of BmMet2 fused with Gal4DBD induced JHdependent activity of an upstream activation sequence reporter. Meanwhile, the kJHRE reporter was activated JH-dependently in HEK293 cells only when cotransfected with BmMet2 and BmSRC, another bHLH-PAS family member, suggesting that BmMet2 and BmSRC jointly interact with kJHRE. We also found that the interaction between BmMet2 and BmSRC is dependent on JH. Therefore, we propose the following hypothesis for the mechanism of JHmediated induction of BmKr-h1: BmMet2 accepts JH as a ligand, JH-liganded BmMet2 interacts with BmSRC, and the JH/BmMet2/ BmSRC complex activates BmKr-h1 by interacting with kJHRE. development | insecticide | steroid receptor coactivator

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“…In Drosophila, metamorphosis is triggered by pulses of the steroid hormone 20-OH ecdysone (ecdysone) (reviewed in refs. [1][2][3][4]. A complex of ecdysone bound to its nuclear receptor, a heterodimer of the ecdysone receptor (EcR) and the RXR ortholog Ultraspiracle (Usp), directly activates a small number of primary response genes, including E93, which in turn regulate many secondary response genes that function more directly in controlling cell fate.…”

mentioning

confidence: 99%

“…To place E93 in the bract pathway, we examined clones homozygous for E93 4 . Such clones show loss or strong reduction of Dll expression in bract cells (Fig.…”

mentioning

confidence: 99%

Control of target gene specificity during metamorphosis by the steroid response gene E93

Mou

Duncan

Baehrecke

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Hormonal control of sexual maturation is a common feature in animal development. A particularly dramatic example is the metamorphosis of insects, in which pulses of the steroid hormone ecdysone drive the wholesale transformation of the larva into an adult. The mechanisms responsible for this transformation are not well understood. Work in Drosophila indicates that the larval and adult forms are patterned by the same underlying sets of developmental regulators, but it is not understood how the same regulators pattern two distinct forms. Recent studies indicate that this ability is facilitated by a global change in the responsiveness of target genes during metamorphosis. Here we show that this shift is controlled in part by the ecdysone-induced transcription factor E93. Although long considered a dedicated regulator of larval cell death, we find that E93 is expressed widely in adult cells at the pupal stage and is required for many patterning processes at this time. To understand the role of E93 in adult patterning, we focused on a simple E93-dependent process, the induction of the Dll gene within bract cells of the pupal leg by EGF receptor signaling. In this system, we show that E93 functions to cause Dll to become responsive to EGF receptor signaling. We demonstrate that E93 is both necessary and sufficient for directing this switch. E93 likely controls the responsiveness of many other target genes because it is required broadly for patterning during metamorphosis. The wide conservation of E93 orthologs suggests that similar mechanisms control life-cycle transitions in other organisms, including vertebrates.Distal-less | Eip93F | epidermal growth factor receptor | ultraspiracle | heterochrony S teroid hormones control metabolism, reproduction, and development in many organisms and have been linked to numerous human health problems. Steroids often control major transitions in the life cycle, regulating distinct cell responses in a stage-specific manner. Despite their global importance in development, relatively little is known about how steroid hormones control such stage-specific responses. One of the most dramatic life-cycle transitions driven by steroids is the metamorphosis of insects, in which there is a wholesale transformation of the larva into the adult. In Drosophila, metamorphosis is triggered by pulses of the steroid hormone 20-OH ecdysone (ecdysone) (reviewed in refs. 1-4). A complex of ecdysone bound to its nuclear receptor, a heterodimer of the ecdysone receptor (EcR) and the RXR ortholog Ultraspiracle (Usp), directly activates a small number of primary response genes, including E93, which in turn regulate many secondary response genes that function more directly in controlling cell fate. The role of ecdysone signaling in early events of metamorphosis, such as the death of larval cells and the morphogenesis of adult structures, has been studied extensively. However, mechanisms underlying the control of adult cell fates by ecdysone have been poorly characterized.In adult cells, many genes seem to un...

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Arthropod nuclear receptors and their role in molting

Cited by 225 publications

References 304 publications

Ecdysone receptor in the mud crab Scylla paramamosain: a possible role in promoting ovarian development

Ecdysone receptor in the mud crab Scylla paramamosain: a possible role in promoting ovarian development

Transcriptional regulation of juvenile hormone-mediated induction of Krüppel homolog 1, a repressor of insect metamorphosis

Control of target gene specificity during metamorphosis by the steroid response gene E93

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