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Lawrence I Gilbert - One of the best experts on this subject based on the ideXlab platform.
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The Insect Neuropeptide PTTH Activates Receptor Tyrosine Kinase Torso to Initiate Metamorphosis
2016Co-Authors: Kim F Rewitz, Naoki Yamanaka, Lawrence I Gilbert, Michael B. O’connorAbstract:Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived Prothoracicotropic Hormone (PTTH), which stimulates the production of the molting Hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal–regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway. Manyorganisms undergo distinct tempo-ral transitions in morphology as a partof their normal life process. In humans, for example, passage through puberty is accompa-nied by changes in body mass and the acquisition of sexual maturity. Likewise, in all holometabolous insects, metamorphosis transforms the immatur
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accessory gland as a site for Prothoracicotropic Hormone controlled ecdysone synthesis in adult male insects
PLOS ONE, 2013Co-Authors: Julie L. Hentze, Lawrence I Gilbert, James T. Warren, Morten E. Moeller, Meghan S. Bengtsson, Anna M. Bordoy, Anne Jorgensen, Ole Andersen, Kim F RewitzAbstract:Insect steroid Hormones (ecdysteroids) are important for female reproduction in many insect species and are required for the initiation and coordination of vital developmental processes. Ecdysteroids are also important for adult male physiology and behavior, but their exact function and site of synthesis remains unclear, although previous studies suggest that the reproductive system may be their source. We have examined expression profiles of the ecdysteroidogenic Halloween genes, during development and in adults of the flour beetle Tribolium castaneum. Genes required for the biosynthesis of ecdysone (E), the precursor of the molting Hormone 20-hydroxyecdysone (20E), are expressed in the tubular accessory glands (TAGs) of adult males. In contrast, expression of the gene encoding the enzyme mediating 20E synthesis was detected in the ovaries of females. Further, Spookiest (Spot), an enzyme presumably required for endowing tissues with competence to produce ecdysteroids, is male specific and predominantly expressed in the TAGs. We also show that Prothoracicotropic Hormone (PTTH), a regulator of E synthesis during larval development, regulates ecdysteroid levels in the adult stage in Drosophila melanogaster and the gene for its receptor Torso seems to be expressed specifically in the accessory glands of males. The composite results suggest strongly that the accessory glands of adult male insects are the main source of E, but not 20E. The finding of a possible male-specific source of E raises the possibility that E and 20E have sex-specific roles analogous to the vertebrate sex steroids, where males produce primarily testosterone, the precursor of estradiol. Furthermore this study provides the first evidence that PTTH regulates ecdysteroid synthesis in the adult stage and could explain the original finding that some adult insects are a rich source of PTTH.
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the insect neuropeptide ptth activates receptor tyrosine kinase torso to initiate metamorphosis
Science, 2009Co-Authors: Kim F Rewitz, Naoki Yamanaka, Lawrence I Gilbert, Michael B OconnorAbstract:Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived Prothoracicotropic Hormone (PTTH), which stimulates the production of the molting Hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal-regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway.
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Protein kinase C modulates ecdysteroidogenesis in the prothoracic gland of the tobacco hornworm, Manduca sexta.
Molecular and Cellular Endocrinology, 2006Co-Authors: Lawrence I GilbertAbstract:The prothoracic gland is the primary source of ecdysteroid Hormones in the immature insect. Ecdysteroids coordinate gene expression necessary for growth, molting and metamorphosis. Prothoracicotropic Hormone (PTTH), a brain neuropeptide, regulates ecdysteroid synthesis in the prothoracic gland. PTTH stimulates ecdysteroid synthesis through a signal transduction cascade that involves at least four protein kinases: protein kinase A (PKA), p70 S6 kinase, an unidentified tyrosine kinase, and the extracellular signal-regulated kinase (ERK). In this report, the participation of protein kinase C (PKC) in PTTH signalling is demonstrated and characterized. PTTH stimulates PKC activity through a PLC and Ca2+-dependent pathway that is not cAMP regulated. Inhibition of PKC inhibits PTTH-stimulated ecdysteroidogenesis as well as PTTH-stimulated phosphorylation of ERK and its upstream regulator, MAP/ERK kinase (MEK). These observations reveal that the acute regulation of prothoracic gland steroidogenesis is dependent on a web of interacting kinase pathways, which probably converge on factors that regulate translation.
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Prothoracicotropic Hormone stimulated extracellular signal regulated kinase erk activity the changing roles of ca2 and camp dependent mechanisms in the insect prothoracic glands during metamorphosis
Molecular and Cellular Endocrinology, 2003Co-Authors: Robert Rybczynski, Lawrence I GilbertAbstract:Abstract The synthesis of ecdysteroids by the lepidopteran prothoracic gland is regulated by a brain neuropeptide Hormone, Prothoracicotropic Hormone (PTTH). In Manduca sexta glands, PTTH stimulates several events including Ca 2+ influx, Ca 2+ -dependent cAMP generation and the activation of several protein kinases. In the present study, the path by which PTTH stimulates extracellular signal-activated regulated kinase (ERK) phosphorylation was investigated using PTTH and second messenger analogs. The results indicate that Ca 2+ -dependent processes, other than cAMP generation, play the major role in PTTH stimulation of ERK phosphorylation in larval prothoracic glands, that cAMP-dependent events increase in importance during later development and that PTTH-stimulated ERK phosphorylation is highest in larval glands. The decline in PTTH-stimulated ERK phosphorylation associated with metamorphosis results from decreased ERK levels and an increased basal rate of ERK phosphorylation. The data suggest that the role or importance of components of the PTTH signal transduction cascade are not fixed and can change during development.
Hiroshi Kataoka - One of the best experts on this subject based on the ideXlab platform.
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Myosuppressin is involved in the regulation of pupal diapause in the cabbage army moth Mamestra brassicae
Scientific Reports, 2017Co-Authors: Nobuto Yamada, Hiroshi Kataoka, Akira MizoguchiAbstract:Diapause, a programmed developmental arrest, is common in insects, enabling them to survive adverse seasons. It is well established that pupal diapause is regulated by ecdysteroids secreted by the prothoracic glands (PGs), with cessation of ecdysteroid secretion after pupal ecdysis leading to pupal diapause. A major factor regulating the gland activity is Prothoracicotropic Hormone (PTTH) secreted from the brain. In our previous study, we demonstrated that the cessation of PTTH release after pupal ecdysis resulted in the inactivation of the PGs, leading to pupal diapause in the cabbage army moth Mamestra brassicae . Here we show that a neuropeptide myosuppressin also contributes to the inactivation of PGs at the initiation of diapause. Myosuppressin suppresses PTTH-stimulated activation of the PGs in vitro . Concentrations of myosuppressin in the hemolymph after pupal ecdysis are higher in diapause pupae than in nondiapause pupae.
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Prothoracicotropic Hormone Acts as a Neuroendocrine Switch between Pupal Diapause and Adult Development
2016Co-Authors: Akira Mizoguchi, Nobuto Yamada, Shintaro Ohsumi, Katuji Kobayashi, Naoki Okamoto, Ken Tateishi, Yoshinori Fujimoto, Hiroshi KataokaAbstract:Diapause is a programmed developmental arrest that has evolved in a wide variety of organisms and allows them survive unfavorable seasons. This developmental state is particularly common in insects. Based on circumstantial evidence, pupal diapause has been hypothesized to result from a cessation of Prothoracicotropic Hormone (PTTH) secretion from the brain. Here, we provide direct evidence for this classical hypothesis by determining both the PTTH titer in the hemolymph and the PTTH content in the brain of diapause pupae in the cabbage army moth Mamestra brassicae. For this purpose, we cloned the PTTH gene, produced PTTH-specific antibodies, and developed a highly sensitive immunoassay for PTTH. While the hemolymph PTTH titer in non-diapause pupae was maintained at high levels after pupation, the titer in diapause pupae dropped to an undetectable level. In contrast, the PTTH content of the post-pupation brain was higher in diapause animals than in non-diapause animals. These results clearly demonstrate that diapause pupae have sufficient PTTH in their brain, but they do not release it into the hemolymph. Injecting PTTH into diapause pupae immediately after pupation induced adult development, showing that a lack of PTTH is a necessary and sufficient condition for inducing pupal diapause. Most interestingly, in diapause-destined larvae, lower hemolymph titers of PTTH and reduced PTTH gene expression were observed for 4 and 2 days, respectively, prior to pupation. This discovery demonstrates that the diapause program is alread
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structural determination of an n glycan moiety attached to the Prothoracicotropic Hormone from the silkmoth bombyx mori
Bioscience Biotechnology and Biochemistry, 2014Co-Authors: Shinji Nagata, Hiroshi Kataoka, Jun Kobayashi, Akinori SuzukiAbstract:The predominant structure of the N-glycan on the Prothoracicotropic Hormone (PTTH) isolated from 1.8 million adult heads of silkmoths was determined to be Manα1-6Manβ1-4GlcNAcβ1-4(Fucα1-6)GlcNAc-OH, which is identical to that of the baculovirus-expressed recombinant PTTH. An ecdysis progression assay demonstrated that N-glycosylated PTTH exhibited a slightly higher activity than the recombinant PTTH without N-glycosylation produced by an Escherichia coli expression system.
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Prothoracicotropic Hormone acts as a neuroendocrine switch between pupal diapause and adult development
PLOS ONE, 2013Co-Authors: Akira Mizoguchi, Nobuto Yamada, Shintaro Ohsumi, Katuji Kobayashi, Naoki Okamoto, Ken Tateishi, Yoshinori Fujimoto, Hiroshi KataokaAbstract:Diapause is a programmed developmental arrest that has evolved in a wide variety of organisms and allows them survive unfavorable seasons. This developmental state is particularly common in insects. Based on circumstantial evidence, pupal diapause has been hypothesized to result from a cessation of Prothoracicotropic Hormone (PTTH) secretion from the brain. Here, we provide direct evidence for this classical hypothesis by determining both the PTTH titer in the hemolymph and the PTTH content in the brain of diapause pupae in the cabbage army moth Mamestra brassicae. For this purpose, we cloned the PTTH gene, produced PTTH-specific antibodies, and developed a highly sensitive immunoassay for PTTH. While the hemolymph PTTH titer in non-diapause pupae was maintained at high levels after pupation, the titer in diapause pupae dropped to an undetectable level. In contrast, the PTTH content of the post-pupation brain was higher in diapause animals than in non-diapause animals. These results clearly demonstrate that diapause pupae have sufficient PTTH in their brain, but they do not release it into the hemolymph. Injecting PTTH into diapause pupae immediately after pupation induced adult development, showing that a lack of PTTH is a necessary and sufficient condition for inducing pupal diapause. Most interestingly, in diapause-destined larvae, lower hemolymph titers of PTTH and reduced PTTH gene expression were observed for 4 and 2 days, respectively, prior to pupation. This discovery demonstrates that the diapause program is already manifested in the PTTH neurons as early as the mid final instar stage.
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Expressions of the cytochrome P450 monooxygenase gene Cyp4g1 and its homolog in the prothoracic glands of the fruit fly Drosophila melanogaster (Diptera: Drosophilidae) and the silkworm Bombyx mori (Lepidoptera: Bombycidae)
Applied Entomology and Zoology, 2011Co-Authors: Ryusuke Niwa, Takashi Sakudoh, Takeshi Matsuya, Toshiki Namiki, Shinji Kasai, Takashi Tomita, Hiroshi KataokaAbstract:Here we describe the expression profiles of the cytochrome P450 monooxygenase gene Cyp4g1 in the fruit fly, Drosophila melanogaster Meigen, and its homolog in the silkworm, Bombyx mori L. We identified Cyp4g1 by a microarray analysis to examine the expression levels of 86 predicted D. melanogaster P450 genes in the ring gland that contains the prothoracic gland (PG), an endocrine organ responsible for synthesizing ecdysteroids. B. mori Cyp4g25 is a closely related homolog of D. melanogaster Cyp4g1 and is also expressed in the PG. A developmental expression pattern of Cyp4g25 in the PG is positively correlated with a fluctuation in hemolymph ecdysteroid titer in the late stage of the final instar. Moreover, the expression of Cyp4g25 in cultured PGs is significantly induced by the addition of Prothoracicotropic Hormone (PTTH), a neuropeptide Hormone that stimulates the synthesis and release of ecdysone. We propose that Cyp4g1 and Cyp4g25 are the candidates that play a role in regulating PG function and control ecdysteroid production and/or metabolism during insect development.
Daryl E Klein - One of the best experts on this subject based on the ideXlab platform.
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structural basis of neuroHormone perception by the receptor tyrosine kinase torso
Molecular Cell, 2015Co-Authors: Simon Jenni, Yogesh Goyal, Marcin Von Grotthuss, Stanislav Y Shvartsman, Daryl E KleinAbstract:In insects, brain-derived Prothoracicotropic Hormone (PTTH) activates the receptor tyrosine kinase (RTK) Torso to initiate metamorphosis through the release of ecdysone. We have determined the crystal structure of silkworm PTTH in complex with the ligand-binding region of Torso. Here we show that ligand-induced Torso dimerization results from the sequential and negatively cooperative formation of asymmetric heterotetramers. Mathematical modeling of receptor activation based upon our biophysical studies shows that ligand pulses are "buffered" at low receptor levels, leading to a sustained signal. By contrast, high levels of Torso develop the signal intensity and duration of a noncooperative system. We propose that this may allow Torso to coordinate widely different functions from a single ligand by tuning receptor levels. Phylogenic analysis indicates that Torso is found outside arthropods, including human parasitic roundworms. Together, our findings provide mechanistic insight into how this receptor system, with roles in embryonic and adult development, is regulated.
Kim F Rewitz - One of the best experts on this subject based on the ideXlab platform.
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The Insect Neuropeptide PTTH Activates Receptor Tyrosine Kinase Torso to Initiate Metamorphosis
2016Co-Authors: Kim F Rewitz, Naoki Yamanaka, Lawrence I Gilbert, Michael B. O’connorAbstract:Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived Prothoracicotropic Hormone (PTTH), which stimulates the production of the molting Hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal–regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway. Manyorganisms undergo distinct tempo-ral transitions in morphology as a partof their normal life process. In humans, for example, passage through puberty is accompa-nied by changes in body mass and the acquisition of sexual maturity. Likewise, in all holometabolous insects, metamorphosis transforms the immatur
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accessory gland as a site for Prothoracicotropic Hormone controlled ecdysone synthesis in adult male insects
PLOS ONE, 2013Co-Authors: Julie L. Hentze, Lawrence I Gilbert, James T. Warren, Morten E. Moeller, Meghan S. Bengtsson, Anna M. Bordoy, Anne Jorgensen, Ole Andersen, Kim F RewitzAbstract:Insect steroid Hormones (ecdysteroids) are important for female reproduction in many insect species and are required for the initiation and coordination of vital developmental processes. Ecdysteroids are also important for adult male physiology and behavior, but their exact function and site of synthesis remains unclear, although previous studies suggest that the reproductive system may be their source. We have examined expression profiles of the ecdysteroidogenic Halloween genes, during development and in adults of the flour beetle Tribolium castaneum. Genes required for the biosynthesis of ecdysone (E), the precursor of the molting Hormone 20-hydroxyecdysone (20E), are expressed in the tubular accessory glands (TAGs) of adult males. In contrast, expression of the gene encoding the enzyme mediating 20E synthesis was detected in the ovaries of females. Further, Spookiest (Spot), an enzyme presumably required for endowing tissues with competence to produce ecdysteroids, is male specific and predominantly expressed in the TAGs. We also show that Prothoracicotropic Hormone (PTTH), a regulator of E synthesis during larval development, regulates ecdysteroid levels in the adult stage in Drosophila melanogaster and the gene for its receptor Torso seems to be expressed specifically in the accessory glands of males. The composite results suggest strongly that the accessory glands of adult male insects are the main source of E, but not 20E. The finding of a possible male-specific source of E raises the possibility that E and 20E have sex-specific roles analogous to the vertebrate sex steroids, where males produce primarily testosterone, the precursor of estradiol. Furthermore this study provides the first evidence that PTTH regulates ecdysteroid synthesis in the adult stage and could explain the original finding that some adult insects are a rich source of PTTH.
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the insect neuropeptide ptth activates receptor tyrosine kinase torso to initiate metamorphosis
Science, 2009Co-Authors: Kim F Rewitz, Naoki Yamanaka, Lawrence I Gilbert, Michael B OconnorAbstract:Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived Prothoracicotropic Hormone (PTTH), which stimulates the production of the molting Hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal-regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway.
Michael B Oconnor - One of the best experts on this subject based on the ideXlab platform.
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Prothoracicotropic Hormone modulates environmental adaptive plasticity through the control of developmental timing
Development, 2018Co-Authors: Mary Jane Shimell, Michael B Oconnor, Xueyang Pan, Francisco A Martin, Arpan C Ghosh, Pierre Leopold, Nuria M RomeroAbstract:Adult size and fitness are controlled by a combination of genetics and environmental cues. In Drosophila, growth is confined to the larval phase and final body size is impacted by the duration of this phase, which is under neuroendocrine control. The neuropeptide Prothoracicotropic Hormone (PTTH) has been proposed to play a central role in controlling the length of the larval phase through regulation of ecdysone production, a steroid Hormone that initiates larval molting and metamorphosis. Here, we test this by examining the consequences of null mutations in the Ptth gene for Drosophila development. Loss of Ptth causes several developmental defects, including a delay in developmental timing, increase in critical weight, loss of coordination between body and imaginal disc growth, and reduced adult survival in suboptimal environmental conditions such as nutritional deprivation or high population density. These defects are caused by a decrease in ecdysone production associated with altered transcription of ecdysone biosynthetic genes. Therefore, the PTTH signal contributes to coordination between environmental cues and the developmental program to ensure individual fitness and survival.
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the insect neuropeptide ptth activates receptor tyrosine kinase torso to initiate metamorphosis
Science, 2009Co-Authors: Kim F Rewitz, Naoki Yamanaka, Lawrence I Gilbert, Michael B OconnorAbstract:Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived Prothoracicotropic Hormone (PTTH), which stimulates the production of the molting Hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal-regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway.
