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Hanswilli Honegger - One of the best experts on this subject based on the ideXlab platform.
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Bursicon-expressing neurons undergo apoptosis after adult ecdysis in the mosquito Anopheles gambiae
Journal of insect physiology, 2011Co-Authors: Hanswilli Honegger, Tania Y. Estévez-lao, Julián F. HillyerAbstract:Neuropeptides are important regulators of diverse processes during development. The insect neuropeptide Bursicon, a 30 kDa heterodimer, controls the hardening of the new cuticle after the shedding of the old one (ecdysis) and the inflation and maturation of adult wings. Given this specific functional role, its expression should only be required transiently because adult insects no longer undergo ecdysis. Here we report the transient expression of Bursicon in the mosquito, Anopheles gambiae. Quantitative RT-PCR revealed that transcription of the Bursicon monomers, burs and pburs, steadily increases through the larval stages, peaks in the black pupa stage, and decreases to below detectable levels by 8 h after adult ecdysis (eclosion). Immunohistochemistry on the adult nervous system showed that Bursicon is co-expressed with crustacean cardioactive peptide (CCAP) in specific neurons of the abdominal ganglia, but that labeling intensity wanes by 14 h post-eclosion. Finally, detection of disintegrating DNA by TUNEL labeling demonstrated that the Bursicon expressing neurons successively undergo apoptosis following eclosion. Taken altogether, these data describe A. gambiae as another holometabolous insect in which Bursicon ceases to be produced in adults, and in which the Bursicon expressing neurons are removed from the ventral nerve cord.
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Bursicon Functions within the Drosophila CNS to Modulate Wing Expansion Behavior, Hormone Secretion, and Cell Death
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008Co-Authors: Nathan C. Peabody, Hanswilli Honegger, Elizabeth M Dewey, Fengqiu Diao, Haojiang Luan, Howard Wang, Benjamin H WhiteAbstract:Hormones are often responsible for synchronizing somatic physiological changes with changes in behavior. Ecdysis (i.e., the shedding of the exoskeleton) in insects has served as a useful model for elucidating the molecular and cellular mechanisms of this synchronization, and has provided numerous insights into the hormonal coordination of body and behavior. An example in which the mechanisms have remained enigmatic is the neurohormone Bursicon, which, after the final molt, coordinates the plasticization and tanning of the initially folded wings with behaviors that drive wing expansion. The somatic effects of the hormone are governed by Bursicon that is released into the blood from neurons in the abdominal ganglion (the B(AG)), which die after wing expansion. How Bursicon induces the behavioral programs required for wing expansion, however, has remained unknown. Here we show by targeted suppression of excitability that a pair of Bursicon-immunoreactive neurons distinct from the B(AG) and located within the subesophageal ganglion in Drosophila (the B(SEG)) is involved in controlling wing expansion behaviors. Unlike the B(AG), the B(SEG) arborize widely in the nervous system, including within the abdominal neuromeres, suggesting that, in addition to governing behavior, they also may modulate the B(AG.) Indeed, we show that animals lacking Bursicon receptor function have deficits both in the humoral release of Bursicon and in posteclosion apoptosis of the B(AG). Our results reveal novel neuromodulatory functions for Bursicon and support the hypothesis that the B(SEG) are essential for orchestrating both the behavioral and somatic processes underlying wing expansion.
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Bursicon, the tanning hormone of insects: recent advances following the discovery of its molecular identity
Journal of Comparative Physiology A, 2008Co-Authors: Hanswilli Honegger, Elizabeth M Dewey, John EwerAbstract:Bursicon was identified in 1965 as a peptide neurohormone that initiates the tanning of the insect cuticle immediately after the shedding of the old one during the final stages of the molting process. Its molecular identity as an approximately 30 kDa bioactive heterodimer consisting of two cystine knot proteins resisted elucidation for 43 years. The sequence of the two Bursicon subunits is highly conserved among arthropods, and this conservation extends even to echinoderms. We review the efforts leading to Bursicon’s characterization, the identification of its leucine-rich repeat-containing, G protein-coupled receptor (LGR2), and the progress towards revealing its various functions. It is now clear that Bursicon regulates different aspects of wing inflation in Drosophila melanogaster besides being involved at various points in the cuticle tanning process in different insects. We also describe the current knowledge of the expression of Bursicon in the central nervous system of different insects in large homologous neurosecretory cells, and the changes in its expression during the development of Manduca sexta and D. melanogaster . Although much remains to be learned, the elucidation of its molecular identity and that of its receptor has provided the breakthrough needed for investigating the diverse actions of this critical insect neurohormone.
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Two peptide transmitters co-packaged in a single neurosecretory vesicle.
Peptides, 2008Co-Authors: Elvin Woodruff, Kendal Broadie, Hanswilli HoneggerAbstract:Numerous neurosecretory cells are known to secrete more than one peptide, in both vertebrates and invertebrates. These co-expressed neuropeptides often originate from differential cleavage of a single large precursor, and are then usually sorted in the regulated pathway into different secretory vesicle classes to allow separable release dynamics. Here, we use immuno-gold electron microscopy to show that two very different neuropeptides (the nonapeptide crustacean cardioactive peptide (CCAP) and the 30 kDa heterodimeric Bursicon) are co-packaged within the same dense core vesicles in neurosecretory neurons in the abdominal ganglia of Periplaneta americana. We suggest that this co-packaging serves a physiological function in which CCAP accelerates the distribution of Bursicon to the epidermis after ecdysis to regulate sclerotization of the newly formed cuticle.
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Identification, developmental expression, and functions of Bursicon in the tobacco hawkmoth, Manduca sexta.
The Journal of comparative neurology, 2008Co-Authors: Li Dai, Hanswilli Honegger, Elizabeth M Dewey, Dusan Zitnan, Ching-wei Luo, Michael E AdamsAbstract:During posteclosion, insects undergo sequential processes of wing expansion and cuticle tanning. Bursicon, a highly conserved neurohormone implicated in regulation of these processes, was characterized recently as a heterodimeric cystine knot protein in Drosophila melanogaster. Here we report the predicted precursor sequences of Bursicon subunits (Masburs and Maspburs) in the moth Manduca sexta. Distinct developmental patterns of mRNA transcript and subunit-specific protein labeling of burs and pburs as well as crustacean cardioactive peptide in neurons of the ventral nervous system were observed in pharate larval, pupal, and adult stages. A subset of Bursicon neurons located in thoracic ganglia of larvae expresses ecdysis-triggering hormone (ETH) receptors, suggesting that they are direct targets of ETH. Projections of Bursicon neurons within the CNS and to neurohemal secretory sites are consistent with both central signaling and circulatory hormone functions. Intrinsic cells of the corpora cardiaca contain pburs transcripts and pburs-like immunoreactivity, whereas burs transcripts and burs-like immunoreactivity were absent in these cells. Recombinant Bursicon induces both wing expansion and tanning, whereas synthetic eclosion hormone induces only wing expansion.
Simon G Webster - One of the best experts on this subject based on the ideXlab platform.
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Identification and expression of mRNAs encoding Bursicon in the plesiomorphic central nervous system of Homarus gammarus.
General and comparative endocrinology, 2010Co-Authors: Jasmine H. Sharp, David C Wilcockson, Simon G WebsterAbstract:Abstract Ecdysis in arthropods is a complex process, regulated by many neurohormones, which must be released in a precisely coordinated manner. In insects, the ultimate hormone involved in this process is the cuticle tanning hormone, Bursicon. Recently, this hormone has been identified in crustaceans. To further define the distribution of Bursicon in crustacean nervous systems, and to compare hormone structures within the sub-phylum, cDNAs encoding both Bursicon subunits were cloned and sequenced from the nervous system of the European lobster, Homarus gammarus , and expression patterns including those for CCAP determined using in-situ hybridisation, quantitative RT-PCR and immunohistochemistry. Full-length cDNAs encoded Bursicon subunits of 121 amino acids (Average M r : 13365.48) for Burs α, 115 amino acids (Average M r : 12928.54) for Burs β. Amino acid sequences were most closely related to those of crabs, and for Burs β the sequence was identical to that of the American lobster, Homarus americanus . Complete co-localisation with CCAP in the VNC was seen. Copy numbers burs α , burs β and CCAP mRNAs were between 0.5 and 1.5 × 10 5 for both Bursicon subunits, 0.5–6 × 10 5 per cdn neurone for CCAP. The terminal abdominal ganglia (AG 6–8) contained about 52 cdn-type neurons, making it the largest Bursicon producing region in the CNS. Double labelling IHC using recombinant Carcinus Burs α and CCAP antisera demonstrated complete co-localisation in the VNC. On the basis of the results obtained, it is proposed that CCAP and Bursicon release occur simultaneously during ecdysis in crustaceans.
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identification and developmental expression of mrnas encoding putative insect cuticle hardening hormone Bursicon in the green shore crab carcinus maenas
General and Comparative Endocrinology, 2008Co-Authors: David C Wilcockson, Simon G WebsterAbstract:Bursicon is the ultimate hormone in insect ecdysis, which is involved in cuticle hardening. Here we show that mRNAs encoding the heterodimeric cystine knot protein Bursicon (Burs α, β), are present in crustaceans, suggesting ubiquity of this hormone in arthropods. We firstly report the cloning, sequencing of mRNAs encoding subunits from the water flea, Daphnia arenata and the CNS of the crab, Carcinus maenas, in comparison with insect Bursicon subunits. Expression patterns of α and β burs mRNAs were examined by in-situ hybridisation (ISH) and quantitative RT-PCR. In the thoracic ganglion, burs α and β mRNAs were completely colocalised in neurones expressing crustacean cardioactive peptide (CCAP). However, in the brain and eyestalk, Bursicon transcripts were never observed, despite a complex expression pattern of CCAP interneurones. Patterns of expression of burs α and β mRNAs were constitutive during the moult cycle of adult crabs, in stark contrast to the situation in insects. Whilst copy numbers of burs β transcripts closely matched those of CCAP, those of burs α mRNA were around 3-fold higher than burs β. This pattern was apparent during embryogenesis, where Bursicon transcripts were first observed at around 50% development—the same time as first expression of CCAP mRNA. Transcript ratios (burs α: β) increased during development. Our studies have shown, for the first time, that Bursicon mRNAs are expressed in identified neurones in the nervous system of crustaceans. These findings will now promote further investigation into the functions of Bursicon during the moult cycle and development of crustaceans.
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identification and developmental expression of mrnas encoding putative insect cuticle hardening hormone Bursicon in the green shore crab carcinus maenas
General and Comparative Endocrinology, 2008Co-Authors: David C Wilcockson, Simon G WebsterAbstract:Bursicon is the ultimate hormone in insect ecdysis, which is involved in cuticle hardening. Here we show that mRNAs encoding the heterodimeric cystine knot protein Bursicon (Burs alpha, beta), are present in crustaceans, suggesting ubiquity of this hormone in arthropods. We firstly report the cloning, sequencing of mRNAs encoding subunits from the water flea, Daphnia arenata and the CNS of the crab, Carcinus maenas, in comparison with insect Bursicon subunits. Expression patterns of alpha and beta burs mRNAs were examined by in-situ hybridisation (ISH) and quantitative RT-PCR. In the thoracic ganglion, burs alpha and beta mRNAs were completely colocalised in neurones expressing crustacean cardioactive peptide (CCAP). However, in the brain and eyestalk, Bursicon transcripts were never observed, despite a complex expression pattern of CCAP interneurones. Patterns of expression of burs alpha and beta mRNAs were constitutive during the moult cycle of adult crabs, in stark contrast to the situation in insects. Whilst copy numbers of burs beta transcripts closely matched those of CCAP, those of burs alpha mRNA were around 3-fold higher than burs beta. This pattern was apparent during embryogenesis, where Bursicon transcripts were first observed at around 50% development-the same time as first expression of CCAP mRNA. Transcript ratios (burs alpha: beta) increased during development. Our studies have shown, for the first time, that Bursicon mRNAs are expressed in identified neurones in the nervous system of crustaceans. These findings will now promote further investigation into the functions of Bursicon during the moult cycle and development of crustaceans.
John Ewer - One of the best experts on this subject based on the ideXlab platform.
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The tanning hormone, Bursicon, does not act directly on the epidermis to tan the Drosophila exoskeleton
BMC Biology, 2020Co-Authors: Justin Flaven-pouchon, Javier V. Alvarez, Candy Rojas, John EwerAbstract:Background In insects, continuous growth requires the periodic replacement of the exoskeleton. Once the remains of the exoskeleton from the previous stage have been shed during ecdysis, the new one is rapidly sclerotized (hardened) and melanized (pigmented), a process collectively known as tanning. The rapid tanning that occurs after ecdysis is critical for insect survival, as it reduces desiccation, and gives the exoskeleton the rigidity needed to support the internal organs and to provide a solid anchor for the muscles. This rapid postecdysial tanning is triggered by the “tanning hormone”, Bursicon. Since Bursicon is released into the hemolymph, it has naturally been assumed that it would act on the epidermal cells to cause the tanning of the overlying exoskeleton. Results Here we investigated the site of Bursicon action in Drosophila by examining the consequences on tanning of disabling the Bursicon receptor (encoded by the rickets gene) in different tissues. To our surprise, we found that rapid tanning does not require rickets function in the epidermis but requires it instead in peptidergic neurons of the ventral nervous system (VNS). Although we were unable to identify the signal that is transmitted from the VNS to the epidermis, we show that neurons that express the Drosophila insulin-like peptide ILP7, but not the ILP7 peptide itself, are involved. In addition, we found that some of the Bursicon targets involved in melanization are different from those that cause sclerotization. Conclusions Our findings show that Bursicon does not act directly on the epidermis to cause the tanning of the overlying exoskeleton but instead requires an intermediary messenger produced by peptidergic neurons within the central nervous system. Thus, this work has uncovered an unexpected layer of control in a process that is critical for insect survival, which will significantly alter the direction of future research aimed at understanding how rapid postecdysial tanning occurs.
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The tanning hormone, Bursicon, does not act directly on the epidermis to tan the Drosophila exoskeleton
BMC biology, 2020Co-Authors: Justin Flaven-pouchon, Javier V. Alvarez, Candy Rojas, John EwerAbstract:In insects, continuous growth requires the periodic replacement of the exoskeleton. Once the remains of the exoskeleton from the previous stage have been shed during ecdysis, the new one is rapidly sclerotized (hardened) and melanized (pigmented), a process collectively known as tanning. The rapid tanning that occurs after ecdysis is critical for insect survival, as it reduces desiccation, and gives the exoskeleton the rigidity needed to support the internal organs and to provide a solid anchor for the muscles. This rapid postecdysial tanning is triggered by the “tanning hormone”, Bursicon. Since Bursicon is released into the hemolymph, it has naturally been assumed that it would act on the epidermal cells to cause the tanning of the overlying exoskeleton. Here we investigated the site of Bursicon action in Drosophila by examining the consequences on tanning of disabling the Bursicon receptor (encoded by the rickets gene) in different tissues. To our surprise, we found that rapid tanning does not require rickets function in the epidermis but requires it instead in peptidergic neurons of the ventral nervous system (VNS). Although we were unable to identify the signal that is transmitted from the VNS to the epidermis, we show that neurons that express the Drosophila insulin-like peptide ILP7, but not the ILP7 peptide itself, are involved. In addition, we found that some of the Bursicon targets involved in melanization are different from those that cause sclerotization. Our findings show that Bursicon does not act directly on the epidermis to cause the tanning of the overlying exoskeleton but instead requires an intermediary messenger produced by peptidergic neurons within the central nervous system. Thus, this work has uncovered an unexpected layer of control in a process that is critical for insect survival, which will significantly alter the direction of future research aimed at understanding how rapid postecdysial tanning occurs.
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Regulation of cuticular hydrocarbon profile maturation by Drosophila tanning hormone, Bursicon, and its interaction with desaturase activity
Insect Biochemistry and Molecular Biology, 2016Co-Authors: Justin Flaven-pouchon, John Ewer, Jean-pierre Farine, Jean-françois FerveurAbstract:Shortly after emergence the exoskeleton (cuticle) of adult insects is rapidly expanded, hardened (sclerotized), and pigmented (melanized). In parallel with this process, the oenocytes, which are large polyploid cells located below the abdominal epidermis, secrete onto the cuticle a cocktail of cuticular hydrocarbons (CHs) and waxes. These improve the waterproofing of the cuticle, and also provide important chemosensory and pheromonal cues linked with gender, age, and species differentiation. The hardening and pigmentation of the new cuticle are controlled by the neurohormone, Bursicon, and its receptor, encoded by the DLGR2 receptor, rickets (rk); by contrast, little is known about the timecourse of changes in CH profile and about the role of Bursicon in this process. Here we show in Drosophila that rk function is also required for the normal maturation of the fly's CH profile, with flies mutant for rk function showing dramatically elevated levels of CHs. Interestingly, this effect is mostly abrogated by mutations in the 119 desaturase encoded by the desaturasel gene, which introduces a first double bond into elongated fatty-acid chains, suggesting that desaturasel acts downstream of rk. In addition, flies mutant for rk showed changes in the absolute and relative levels of specific 7-monoenes (in males) and 7,11-dienes (in females). The fact that these differences in CH amounts were obtained using extractions of very different durations suggests that the particular CH profile of flies mutant for rk is not simply due to their unsclerotized cuticle but that Bursicon may be involved in the process of CH biosynthesis itself.
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Cellular/Molecular Genetic Analysis of Ecdysis Behavior in Drosophila Reveals Partially Overlapping Functions of Two Unrelated
2016Co-Authors: Eleanor C. Lahr, Derek Dean, John EwerAbstract:Ecdysis behavior allows insects to shed their old exoskeleton at the end of every molt. It is controlled by a suite of interacting hormones and neuropeptides, and has served as a useful behavior for understanding how bioactive peptides regulate CNS function. Previous findings suggest that crustacean cardioactive peptide (CCAP) activates the ecdysis motor program; the hormone Bursicon is believed to then act downstreamofCCAP to inflate, pigment, andharden the exoskeletonof thenext stage.However, the exact roles of these signaling molecules in regulating ecdysis remain unclear. Here we use a genetic approach to investigate the functions of CCAP and Bursicon in Drosophila ecdysis.We show that nullmutants inCCAPexpress no apparent defects in ecdysis andpostecdysis, producingnormal adults. By contrast, a substantial fraction of flies genetically null for one of the two subunits of Bursicon [encoded by the partner of Bursicon gene (pburs)] show severe defects in ecdysis, with escaper adults exhibiting the expected failures in wing expansion and exoskeleton pigmen-tation andhardening. Furthermore, flies lacking bothCCAPandBursicon showmuchmore severe defects at ecdysis than do animals null for either neuropeptide alone.Our results show that the functions thought tobe subservedbyCCAParepartially effectedbyBursicon, and that Bursicon plays an important and heretofore undescribed role in ecdysis behavior itself. These findings have important implications for understanding the regulation of this vital insect behavior and the mechanisms by which hormones and neuropeptides control the physiology and behavior of animals
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Genetic Analysis of Ecdysis Behavior in Drosophila Reveals Partially Overlapping Functions of Two Unrelated Neuropeptides
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012Co-Authors: Eleanor C. Lahr, Derek M. Dean, John EwerAbstract:Ecdysis behavior allows insects to shed their old exoskeleton at the end of every molt. It is controlled by a suite of interacting hormones and neuropeptides, and has served as a useful behavior for understanding how bioactive peptides regulate CNS function. Previous findings suggest that crustacean cardioactive peptide (CCAP) activates the ecdysis motor program; the hormone Bursicon is believed to then act downstream of CCAP to inflate, pigment, and harden the exoskeleton of the next stage. However, the exact roles of these signaling molecules in regulating ecdysis remain unclear. Here we use a genetic approach to investigate the functions of CCAP and Bursicon in Drosophila ecdysis. We show that null mutants in CCAP express no apparent defects in ecdysis and postecdysis, producing normal adults. By contrast, a substantial fraction of flies genetically null for one of the two subunits of Bursicon [encoded by the partner of Bursicon gene (pburs)] show severe defects in ecdysis, with escaper adults exhibiting the expected failures in wing expansion and exoskeleton pigmentation and hardening. Furthermore, flies lacking both CCAP and Bursicon show much more severe defects at ecdysis than do animals null for either neuropeptide alone. Our results show that the functions thought to be subserved by CCAP are partially effected by Bursicon, and that Bursicon plays an important and heretofore undescribed role in ecdysis behavior itself. These findings have important implications for understanding the regulation of this vital insect behavior and the mechanisms by which hormones and neuropeptides control the physiology and behavior of animals.
Elizabeth M Dewey - One of the best experts on this subject based on the ideXlab platform.
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Bursicon Functions within the Drosophila CNS to Modulate Wing Expansion Behavior, Hormone Secretion, and Cell Death
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008Co-Authors: Nathan C. Peabody, Hanswilli Honegger, Elizabeth M Dewey, Fengqiu Diao, Haojiang Luan, Howard Wang, Benjamin H WhiteAbstract:Hormones are often responsible for synchronizing somatic physiological changes with changes in behavior. Ecdysis (i.e., the shedding of the exoskeleton) in insects has served as a useful model for elucidating the molecular and cellular mechanisms of this synchronization, and has provided numerous insights into the hormonal coordination of body and behavior. An example in which the mechanisms have remained enigmatic is the neurohormone Bursicon, which, after the final molt, coordinates the plasticization and tanning of the initially folded wings with behaviors that drive wing expansion. The somatic effects of the hormone are governed by Bursicon that is released into the blood from neurons in the abdominal ganglion (the B(AG)), which die after wing expansion. How Bursicon induces the behavioral programs required for wing expansion, however, has remained unknown. Here we show by targeted suppression of excitability that a pair of Bursicon-immunoreactive neurons distinct from the B(AG) and located within the subesophageal ganglion in Drosophila (the B(SEG)) is involved in controlling wing expansion behaviors. Unlike the B(AG), the B(SEG) arborize widely in the nervous system, including within the abdominal neuromeres, suggesting that, in addition to governing behavior, they also may modulate the B(AG.) Indeed, we show that animals lacking Bursicon receptor function have deficits both in the humoral release of Bursicon and in posteclosion apoptosis of the B(AG). Our results reveal novel neuromodulatory functions for Bursicon and support the hypothesis that the B(SEG) are essential for orchestrating both the behavioral and somatic processes underlying wing expansion.
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Bursicon, the tanning hormone of insects: recent advances following the discovery of its molecular identity
Journal of Comparative Physiology A, 2008Co-Authors: Hanswilli Honegger, Elizabeth M Dewey, John EwerAbstract:Bursicon was identified in 1965 as a peptide neurohormone that initiates the tanning of the insect cuticle immediately after the shedding of the old one during the final stages of the molting process. Its molecular identity as an approximately 30 kDa bioactive heterodimer consisting of two cystine knot proteins resisted elucidation for 43 years. The sequence of the two Bursicon subunits is highly conserved among arthropods, and this conservation extends even to echinoderms. We review the efforts leading to Bursicon’s characterization, the identification of its leucine-rich repeat-containing, G protein-coupled receptor (LGR2), and the progress towards revealing its various functions. It is now clear that Bursicon regulates different aspects of wing inflation in Drosophila melanogaster besides being involved at various points in the cuticle tanning process in different insects. We also describe the current knowledge of the expression of Bursicon in the central nervous system of different insects in large homologous neurosecretory cells, and the changes in its expression during the development of Manduca sexta and D. melanogaster . Although much remains to be learned, the elucidation of its molecular identity and that of its receptor has provided the breakthrough needed for investigating the diverse actions of this critical insect neurohormone.
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Identification, developmental expression, and functions of Bursicon in the tobacco hawkmoth, Manduca sexta.
The Journal of comparative neurology, 2008Co-Authors: Li Dai, Hanswilli Honegger, Elizabeth M Dewey, Dusan Zitnan, Ching-wei Luo, Michael E AdamsAbstract:During posteclosion, insects undergo sequential processes of wing expansion and cuticle tanning. Bursicon, a highly conserved neurohormone implicated in regulation of these processes, was characterized recently as a heterodimeric cystine knot protein in Drosophila melanogaster. Here we report the predicted precursor sequences of Bursicon subunits (Masburs and Maspburs) in the moth Manduca sexta. Distinct developmental patterns of mRNA transcript and subunit-specific protein labeling of burs and pburs as well as crustacean cardioactive peptide in neurons of the ventral nervous system were observed in pharate larval, pupal, and adult stages. A subset of Bursicon neurons located in thoracic ganglia of larvae expresses ecdysis-triggering hormone (ETH) receptors, suggesting that they are direct targets of ETH. Projections of Bursicon neurons within the CNS and to neurohemal secretory sites are consistent with both central signaling and circulatory hormone functions. Intrinsic cells of the corpora cardiaca contain pburs transcripts and pburs-like immunoreactivity, whereas burs transcripts and burs-like immunoreactivity were absent in these cells. Recombinant Bursicon induces both wing expansion and tanning, whereas synthetic eclosion hormone induces only wing expansion.
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Bursicon the insect cuticle hardening hormone is a heterodimeric cystine knot protein that activates g protein coupled receptor lgr2
Proceedings of the National Academy of Sciences of the United States of America, 2005Co-Authors: Ching-wei Luo, Hanswilli Honegger, Elizabeth M Dewey, John Ewer, Satoko Sudo, Sheau Yu Hsu, Aaron J W HsuehAbstract:All arthropods periodically molt to replace their exoskeleton (cuticle). Immediately after shedding the old cuticle, the neurohormone Bursicon causes the hardening and darkening of the new cuticle. Here we show that Bursicon, to our knowledge the first heterodimeric cystine knot hormone found in insects, consists of two proteins encoded by the genes burs and pburs (partner of burs). The pburs/burs heterodimer from Drosophila melanogaster binds with high affinity and specificity to activate the G protein-coupled receptor DLGR2, leading to the stimulation of cAMP signaling in vitro and tanning in neck-ligated blowflies. Native Bursicon from Periplaneta americana is also a heterodimer. In D. melanogaster the levels of pburs, burs, and DLGR2 transcripts are increased before ecdysis, consistent with their role in postecdysial cuticle changes. Immunohistochemical analyses in diverse insect species revealed the colocalization of pburs- and burs-immunoreactivity in some of the neurosecretory neurons that also express crustacean cardioactive peptide. Forty-three years after its initial description, the elucidation of the molecular identity of Bursicon and the verification of its receptor allow for studies of Bursicon actions in regulating cuticle tanning, wing expansion, and as yet unknown functions. Because Bursicon subunit genes are homologous to the vertebrate bone morphogenetic protein antagonists, our findings also facilitate investigation on the function of these proteins during vertebrate development.
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identification of the gene encoding Bursicon an insect neuropeptide responsible for cuticle sclerotization and wing spreading
Current Biology, 2004Co-Authors: Elizabeth M Dewey, James W. Truman, Susan L Mcnabb, John Ewer, Christina L Takanishi, Hanswilli HoneggerAbstract:To accommodate growth, insects must periodically replace their exoskeletons. After shedding the old cuticle, the new soft cuticle must sclerotize. Sclerotization has long been known to be controlled by the neuropeptide hormone Bursicon [1, 2], but its large size of 30 kDa has frustrated attempts to determine its sequence and structure. Using partial sequences obtained from purified cockroach Bursicon [3], we identified the Drosophila melanogaster gene CG13419 as a candidate Bursicon gene. CG13419 encodes a peptide with a predicted final molecular weight of 15 kDa, which likely functions as a dimer. This predicted Bursicon protein belongs to the cystine knot family, which includes vertebrate transforming growth factor-β (TGF-β) and glycoprotein hormones [4]. Point mutations in the Bursicon gene cause defects in cuticle sclerotization and wing expansion behavior. Bioassays show that these mutants have decreased Bursicon bioactivity. In situ hybridization and immunocytochemistry revealed that Bursicon is co-expressed with crustacean cardioactive peptide (CCAP). Transgenic flies that lack CCAP neurons [5] also lacked Bursicon bioactivity. Our results indicate that CG13419 encodes Bursicon, the last of the classic set of insect developmental hormones. It is the first member of the cystine knot family to have a defined function in invertebrates. Mutants show that the spectrum of Bursicon actions is broader than formerly demonstrated.
Barbara Kostron - One of the best experts on this subject based on the ideXlab platform.
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cellular localization of Bursicon using antisera against partial peptide sequences of this insect cuticle sclerotizing neurohormone
The Journal of Comparative Neurology, 2002Co-Authors: Hanswilli Honegger, Daniel Market, Elizabeth M Dewey, Barbara Kostron, Dennis C Choi, Kathleen A Klukas, Melanie Wilson, Larry Pierce, Karen A MesceAbstract:Bursicon is the final neurohormone released at the end of the molting cycle. It triggers the sclerotization (tanning) of the insect cuticle. Until now, its existence has been verified only by bioassays. In an attempt to identify this important neurohormone, Bursicon was purified from homogenates of 2,850 nerve cords of the cockroach Periplaneta americana by using high performance liquid chromatography technology and two-dimensional gel electrophoresis. Bursicon bioactivity was found in four distinct protein spots at approximately 30 kDa between pH 5.3 and 5.9. The protein of one of these spots at pH 5.7 was subsequently microsequenced, and five partial amino acid sequences were retrieved. Evidence is presented that two of these sequences are derived from Bursicon. Antibodies raised against the two sequences labeled Bursicon-containing neurons in the central nervous systems of P. americana. One of these antisera labeled Bursicon-containing neurons in the crickets Teleogryllus commodus and Gryllus bimaculatus, and the moth Manduca sexta. A cluster of four bilaterally paired neurons in the brain of Drososphila melanogaster was also labeled. In addition, this antiserum detected three spots corresponding to Bursicon in Western blots of two-dimensional gels. The 12-amino acid sequence detected by this antiserum, thus, seems to be conserved even among species that are distantly related. J. Comp. Neurol. 452:163–177, 2002. © 2002 Wiley-Liss, Inc.
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Cellular localization of Bursicon using antisera against partial peptide sequences of this insect cuticle-sclerotizing neurohormone.
The Journal of comparative neurology, 2002Co-Authors: Hanswilli Honegger, Daniel Market, Elizabeth M Dewey, Barbara Kostron, Dennis C Choi, Kathleen A Klukas, Melanie Wilson, Larry Pierce, Karen A MesceAbstract:Bursicon is the final neurohormone released at the end of the molting cycle. It triggers the sclerotization (tanning) of the insect cuticle. Until now, its existence has been verified only by bioassays. In an attempt to identify this important neurohormone, Bursicon was purified from homogenates of 2,850 nerve cords of the cockroach Periplaneta americana by using high performance liquid chromatography technology and two-dimensional gel electrophoresis. Bursicon bioactivity was found in four distinct protein spots at approximately 30 kDa between pH 5.3 and 5.9. The protein of one of these spots at pH 5.7 was subsequently microsequenced, and five partial amino acid sequences were retrieved. Evidence is presented that two of these sequences are derived from Bursicon. Antibodies raised against the two sequences labeled Bursicon-containing neurons in the central nervous systems of P. americana. One of these antisera labeled Bursicon-containing neurons in the crickets Teleogryllus commodus and Gryllus bimaculatus, and the moth Manduca sexta. A cluster of four bilaterally paired neurons in the brain of Drososphila melanogaster was also labeled. In addition, this antiserum detected three spots corresponding to Bursicon in Western blots of two-dimensional gels. The 12-amino acid sequence detected by this antiserum, thus, seems to be conserved even among species that are distantly related.
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Antisera against Periplaneta americana Cu,Zn-superoxide dismutase (SOD): separation of the neurohormone Bursicon from SOD, and immunodetection of SOD in the central nervous system.
Insect biochemistry and molecular biology, 1999Co-Authors: Barbara Kostron, Daniel Market, Josef Kellermann, C.e Carter, Hanswilli HoneggerAbstract:In an effort to characterize the insect molting hormone Bursicon from the cockroach, Periplaneta americana, amino acid sequences with high identity of Cu,Zn-superoxide dismutase (SOD) of Drosophila virilis were identified. Antisera against a conserved region of SOD, and a sequence unique to Periplaneta SOD were produced and used to test whether Bursicon might be a form of SOD. Western blots of one- and two-dimensional gels revealed that the dimeric form of SOD and Bursicon have a similar molecular mass (30 kDa). The two proteins can be separated, however, according to their different isoelectric points. Bursicon is identified in two-dimensional gels by elution from four unique spots not labeled by the anti-SOD antisera. In sections of Periplaneta nerve cords the antisera labeled glial material surrounding neuronal somata close to the neural sheath. Bursicon, however, is contained in unique cell pairs in the ganglia of the ventral nerve cord. These neurons were labeled with new antisera produced against novel sequences of one of the four above-mentioned Bursicon active spots. The results show unequivocally that SOD and Bursicon are distinctly different proteins. Furthermore, the anti-SOD antisera provided a tool to isolate and sequence Bursicon.
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Bursicon, the cuticle sclerotizing hormone - comparison of its molecular mass in different insects
Journal of Insect Physiology, 1995Co-Authors: Barbara Kostron, Ulrike Kaltenhauser, Kathi Marquardt, Hanswilli HoneggerAbstract:Abstract We have shown in a recent study that Bursicon, which induces the tanning of the cuticle in freshly molted insects, is a 30 kDa protein in the meal beetle Tenebrio molitor . We now show that Bursicon in the insect species Calliphora erythrocephala, Periplaneta americana, Gryllus bimaculatus and Locusta migratoria is also a protein of about 30 kDa. The determination of Bursicon's molecular mass was accomplished by SDS-PAGE of nervous system homogenates, subsequent division of the gel into slices, protein elution from these slices, and a test for Bursicon activity of the eluted proteins in the ligated fly bioassay. Bursicon activity can only be eluted from one gel slice spanning the molecular mass around 30 kDa. Dose-response curves for Bursicon of different ventral ganglia show that there are appreciable differences in the Bursicon content between thoracic and abdominal ganglia and between developmental stages. These differences vary from insect to insect. An attempt to determine the molecular mass of Manduca sexta Bursicon was not possible because the ligated fly bioassay does not work with homogenates of the nervous system of Manduca . Homogenates of abdominal ganglia of Homarus americanus show a positive score in the ligated fly bioassay but not those of its thoracic ganglia. The results indicate that Bursicon may have a similar structure throughout the arthropods, but with distinct exceptions.
