DPP-mediated TGFβ signaling regulates juvenile hormone biosynthesis by activating the expression of juvenile hormone acid methyltransferase

Huang, Jianhua; Tian, Ling; Peng, Cheng Yuan; Abdou, Mohamed; Wen, Di; Wang, Ying; Li, Sheng; Wang, Jian

doi:10.1242/dev.057687

Cited by 78 publications

(87 citation statements)

References 41 publications

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“…The overexpression of Z1-3 caused AMPs and PCs to prematurely differentiate into Pdm1-positive EC-like cells, whereas overexpression of Z4 did not affect the timing of AMP/PC differentiation. These results are consistent with a recent report that found that only the Z1-3 isoforms are expressed in larvae (Huang et al, 2011). We only showed data of overexpressing br Z3 in the text.…”

Section: Fly Strainssupporting

confidence: 93%

“…Although the detailed molecular mechanisms of JH and 20E action remain elusive, accumulated evidence suggests that their effects converge on a key transcriptional regulator, Broad (Br, also called BroadComplex or BR-C). The expression of br is directly induced by 20E but inhibited by JH (Huang et al, 2011;Konopova and Jindra, 2008;Suzuki et al, 2008;Zhou et al, 1998;Zhou and Riddiford, 2002). Flies with a loss-of-function br mutation develop normally to the end of L3, but they do not enter the pupal stage (Kiss et al, 1988;Restifo and White, 1991).…”

Section: Introductionmentioning

confidence: 99%

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Broad relays hormone signals to regulate stem cell differentiation in Drosophila midgut during metamorphosis

Zeng

Hou

2012

Development

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SUMMARYLike the mammalian intestine, the Drosophila adult midgut is constantly replenished by multipotent intestinal stem cells (ISCs). Although it is well known that adult ISCs arise from adult midgut progenitors (AMPs), relatively little is known about the mechanisms that regulate AMP specification. Here, we demonstrate that Broad (Br)-mediated hormone signaling regulates AMP specification. Br is highly expressed in AMPs temporally during the larva-pupa transition stage, and br loss of function blocks AMP differentiation. Furthermore, Br is required for AMPs to develop into functional ISCs. Conversely, br overexpression drives AMPs toward premature differentiation. In addition, we found that Br and Notch (N) signaling function in parallel pathways to regulate AMP differentiation. Our results reveal a molecular mechanism whereby Br-mediated hormone signaling directly regulates stem cells to generate adult cells during metamorphosis.

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Section: Fly Strainssupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Broad relays hormone signals to regulate stem cell differentiation in Drosophila midgut during metamorphosis

Zeng

Hou

2012

Development

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“…In Drosophila melanogaster (Dm), it was reported that loss of Dm'mad, Dm'tkv, or Dm'dpp caused precocious metamorphosis, even in the early larval stages (20). Therefore, we first examined whether Dpp signaling plays a role in regulating Gryllus metamorphosis.…”

Section: Resultsmentioning

confidence: 99%

TGF-β signaling in insects regulates metamorphosis via juvenile hormone biosynthesis

Ishimaru

Tomonari

Matsuoka

et al. 2016

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

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Although butterflies undergo a dramatic morphological transformation from larva to adult via a pupal stage (holometamorphosis), crickets undergo a metamorphosis from nymph to adult without formation of a pupa (hemimetamorphosis). Despite these differences, both processes are regulated by common mechanisms that involve 20-hydroxyecdysone (20E) and juvenile hormone (JH). JH regulates many aspects of insect physiology, such as development, reproduction, diapause, and metamorphosis. Consequently, strict regulation of JH levels is crucial throughout an insect’s life cycle. However, it remains unclear how JH synthesis is regulated. Here, we report that in the corpora allata of the cricket, Gryllus bimaculatus, Myoglianin (Gb’Myo), a homolog of Drosophila Myoglianin/vertebrate GDF8/11, is involved in the down-regulation of JH production by suppressing the expression of a gene encoding JH acid O-methyltransferase, Gb’jhamt. In contrast, JH production is up-regulated by Decapentaplegic (Gb’Dpp) and Glass-bottom boat/60A (Gb’Gbb) signaling that occurs as part of the transcriptional activation of Gb’jhamt. Gb’Myo defines the nature of each developmental transition by regulating JH titer and the interactions between JH and 20E. When Gb’myo expression is suppressed, the activation of Gb’jhamt expression and secretion of 20E induce molting, thereby leading to the next instar before the last nymphal instar. Conversely, high Gb’myo expression induces metamorphosis during the last nymphal instar through the cessation of JH synthesis. Gb’myo also regulates final insect size. Because Myo/GDF8/11 and Dpp/bone morphogenetic protein (BMP)2/4-Gbb/BMP5–8 are conserved in both invertebrates and vertebrates, the present findings provide common regulatory mechanisms for endocrine control of animal development.

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“…JH-mediated repression of the activation of BR-C by 20E has been also reported in cultured insect epidermis, but the inhibitory effect of JH declined after the transition to the pupal commitment phase (30,35). A study using the Kr-h1 mutant of Drosophila melanogaster showed that Kr-h1 was required for the repression of BR-C expression in the fat body of young D. melanogaster larvae (36); however, the molecular mechanism underlying the JH-mediated repression of BR-C, particularly whether the BR-C expression is directly repressed by Kr-h1 or repressed by Kr-h1-inducible gene(s), has remained unclear.…”

mentioning

confidence: 77%

Krüppel Homolog 1 Inhibits Insect Metamorphosis via Direct Transcriptional Repression of Broad-Complex, a Pupal Specifier Gene

Kayukawa

Nagamine

Ito

et al. 2016

Journal of Biological Chemistry

120

124

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The Broad-Complex gene (BR-C) encodes transcription factors that dictate larval-pupal metamorphosis in insects. The expression of BR-C is induced by molting hormone (20-hydroxyecdysone (20E)), and this induction is repressed by juvenile hormone (JH), which exists during the premature larval stage. Krüppel homolog 1 gene (Kr-h1) has been known as a JH-early inducible gene responsible for repression of metamorphosis; however, the functional relationship between Kr-h1 and repression of BR-C has remained unclear. To elucidate this relationship, we analyzed cis-and trans elements involved in the repression of BR-C using a Bombyx mori cell line. In the cells, as observed in larvae, JH induced the expression of Kr-h1 and concurrently suppressed 20E-induced expression of BR-C. Forced expression of Kr-h1 repressed the 20E-dependent activation of the BR-C promoter in the absence of JH, and Kr-h1 RNAi inhibited the JH-mediated repression, suggesting that Kr-h1 controlled the repression of BR-C. A survey of the upstream sequence of BR-C gene revealed a Kr-h1 binding site (KBS) in the BR-C promoter. When KBS was deleted from the promoter, the repression of BR-C was abolished. Electrophoresis mobility shift demonstrated that two Kr-h1 molecules bound to KBS in the BR-C promoter. Based on these results, we conclude that Kr-h1 protein molecules directly bind to the KBS sequence in the BR-C promoter and thereby repress 20E-dependent activation of the pupal specifier, BR-C. This study has revealed a considerable portion of the picture of JH signaling pathways from the reception of JH to the repression of metamorphosis.The molting and metamorphosis of insects are intricately regulated by the actions and interactions of ecdysteroids and juvenile hormone (JH).2 In holometabolous insects, 20-hydroxyecdysone (20E, the primary active ecdysteroid) induces the larval-larval molt in the presence of JH. When the JH titer declines to a trace level in the final larval instar, 20E induces larval-pupal and pupal-adult molts (metamorphosis). Thus, JH plays a key role in preventing larvae from undergoing precocious metamorphosis (1).Our understanding of the molecular mechanism of JH-mediated repression of insect metamorphosis has significantly advanced (2): JH carried to a target cell is received by a JH receptor, methoprene tolerant (Met) (3-6); JH-liganded Met interacts with steroid receptor coactivator (7-12); the JH/Met/ steroid receptor coactivator complex activates Krüppel homolog 1 (Kr-h1), a repressor of metamorphosis, by interacting with a JH response element (kJHRE) in the Kr-h1 gene (9, 10, 12-15); Kr-h1 represses the larval-pupal metamorphosis (16 -20). To date, however, the mechanism of the repression of metamorphosis by Kr-h1, including target gene(s), binding site(s), and partner(s), has remained unknown.The Broad-Complex (BR-C) protein is a transcription factor that is composed of a Bric-a-brac/Tramtrack/Broad-Complex (BTB) domain and an alternatively spliced zinc finger domain (Z1-Z6) (21-25). BR-C expression is induced by 20E, ...

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DPP-mediated TGFβ signaling regulates juvenile hormone biosynthesis by activating the expression of juvenile hormone acid methyltransferase

Cited by 78 publications

References 41 publications

Broad relays hormone signals to regulate stem cell differentiation in Drosophila midgut during metamorphosis

Broad relays hormone signals to regulate stem cell differentiation in Drosophila midgut during metamorphosis

TGF-β signaling in insects regulates metamorphosis via juvenile hormone biosynthesis

Krüppel Homolog 1 Inhibits Insect Metamorphosis via Direct Transcriptional Repression of Broad-Complex, a Pupal Specifier Gene

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