Relevant bibliographies by topics / Drosophila models

Academic literature on the topic 'Drosophila models'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Drosophila models"

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Sang, Tzu-Kang, and George R. Jackson. "Drosophila models of neurodegenerative disease." NeuroRX 2, no. 3 (July 2005): 438–46. http://dx.doi.org/10.1602/neurorx.2.3.438.

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Cheng, Louise, Antonio Baonza, and Daniela Grifoni. "Drosophila Models of Human Disease." BioMed Research International 2018 (August 30, 2018): 1–2. http://dx.doi.org/10.1155/2018/7214974.

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Rooney, T. M., and M. R. Freeman. "Drosophila Models of Neuronal Injury." ILAR Journal 54, no. 3 (January 1, 2014): 291–95. http://dx.doi.org/10.1093/ilar/ilt057.

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Wu, Mark N., and Thomas E. Lloyd. "Drosophila models of neurologic disease." Experimental Neurology 274 (December 2015): 1–3. http://dx.doi.org/10.1016/j.expneurol.2015.10.004.

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Vidal, Marcos, and Ross L. Cagan. "Drosophila models for cancer research." Current Opinion in Genetics & Development 16, no. 1 (February 2006): 10–16. http://dx.doi.org/10.1016/j.gde.2005.12.004.

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Millet-Boureima, Cassandra, Caroline C. Ennis, Jurnee Jamison, Shana McSweeney, Anna Park, and Chiara Gamberi. "Empowering Melatonin Therapeutics with Drosophila Models." Diseases 9, no. 4 (September 26, 2021): 67. http://dx.doi.org/10.3390/diseases9040067.

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Melatonin functions as a central regulator of cell and organismal function as well as a neurohormone involved in several processes, e.g., the regulation of the circadian rhythm, sleep, aging, oxidative response, and more. As such, it holds immense pharmacological potential. Receptor-mediated melatonin function mainly occurs through MT1 and MT2, conserved amongst mammals. Other melatonin-binding proteins exist. Non-receptor-mediated activities involve regulating the mitochondrial function and antioxidant cascade, which are frequently affected by normal aging as well as disease. Several pathologies display diseased or dysfunctional mitochondria, suggesting melatonin may be used therapeutically. Drosophila models have extensively been employed to study disease pathogenesis and discover new drugs. Here, we review the multiple functions of melatonin through the lens of functional conservation and model organism research to empower potential melatonin therapeutics to treat neurodegenerative and renal diseases.
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Nagoshi, Emi. "Drosophila Models of Sporadic Parkinson’s Disease." International Journal of Molecular Sciences 19, no. 11 (October 26, 2018): 3343. http://dx.doi.org/10.3390/ijms19113343.

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Parkinson’s disease (PD) is the most common cause of movement disorders and is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. It is increasingly recognized as a complex group of disorders presenting widely heterogeneous symptoms and pathology. With the exception of the rare monogenic forms, the majority of PD cases result from an interaction between multiple genetic and environmental risk factors. The search for these risk factors and the development of preclinical animal models are in progress, aiming to provide mechanistic insights into the pathogenesis of PD. This review summarizes the studies that capitalize on modeling sporadic (i.e., nonfamilial) PD using Drosophila melanogaster and discusses their methodologies, new findings, and future perspectives.
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Calap-Quintana, P., J. A. Navarro, J. González-Fernández, M. J. Martínez-Sebastián, M. D. Moltó, and J. V. Llorens. "Drosophila melanogaster Models of Friedreich’s Ataxia." BioMed Research International 2018 (2018): 1–20. http://dx.doi.org/10.1155/2018/5065190.

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Friedreich’s ataxia (FRDA) is a rare inherited recessive disorder affecting the central and peripheral nervous systems and other extraneural organs such as the heart and pancreas. This incapacitating condition usually manifests in childhood or adolescence, exhibits an irreversible progression that confines the patient to a wheelchair, and leads to early death. FRDA is caused by a reduced level of the nuclear-encoded mitochondrial protein frataxin due to an abnormal GAA triplet repeat expansion in the first intron of the human FXN gene. FXN is evolutionarily conserved, with orthologs in essentially all eukaryotes and some prokaryotes, leading to the development of experimental models of this disease in different organisms. These FRDA models have contributed substantially to our current knowledge of frataxin function and the pathogenesis of the disease, as well as to explorations of suitable treatments. Drosophila melanogaster, an organism that is easy to manipulate genetically, has also become important in FRDA research. This review describes the substantial contribution of Drosophila to FRDA research since the characterization of the fly frataxin ortholog more than 15 years ago. Fly models have provided a comprehensive characterization of the defects associated with frataxin deficiency and have revealed genetic modifiers of disease phenotypes. In addition, these models are now being used in the search for potential therapeutic compounds for the treatment of this severe and still incurable disease.
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Chan, H. Y. E., and N. M. Bonini. "Drosophila models of human neurodegenerative disease." Cell Death & Differentiation 7, no. 11 (November 2000): 1075–80. http://dx.doi.org/10.1038/sj.cdd.4400757.

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Brace, E. J., and Aaron DiAntonio. "Models of axon regeneration in Drosophila." Experimental Neurology 287 (January 2017): 310–17. http://dx.doi.org/10.1016/j.expneurol.2016.03.014.

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Dissertations / Theses on the topic "Drosophila models"

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Zhang, Yan. "Implementation of anti-apoptotic peptide aptamers in cell and "in vivo" models of Parkinson's disease." Thesis, Lyon, École normale supérieure, 2012. http://www.theses.fr/2012ENSL0788.

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La maladie de Parkinson (PD) est considérée comme la deuxième maladie neurodégénérative la plus fréquente. L'examen post-mortem de patients parkinsoniens et des modèles physiologiques d’études de la maladie de Parkinson suggèrent la participation de la mort cellulaire programmée, l'inflammation et l'autophagie dues au stress oxydatif, à des mutations ou l’agrégation de protéines au sein des neurones DA. Les aptamères peptidiques sont de petites protéines combinatoires, consistitués d’une plateforme (dans notre cas, la thiorédoxine humaine, hTRX) et une boucle variable insérée dans le domaine actif de hTRX. Deux aptamères peptidiques ont été identifiés par la sélection fonctionnelle. L’aptamère peptide 32 (Apta-32) ,est spécifique liant deux paralogues T32 impliqués dans le processus d'endocytose. L’aptamère peptidique 34(Apta-34) lie à une cible "T34", une protéine pro-apoptotique ayant un rôle dans la voie apoptotique provenant du noyau. Le travail de cette thèse visait à étudier la fonction anti-apoptotique de nos deux aptamères peptidiques dans deux modèles d’étude de la maladie de Parkinson: un modèle cellulaire (in vitro) et un modèle transgénique D. melanogaster (in vivo). Deux toxines majeures ont été appliquées dans ce travail, 6-hydroxindopamine (6-OHDA) et le paraquat, un pesticide couramment utilisé. Nos observations montrent que la drosophile exprimant Apta-32 dans tous les neurones ont montré une meilleure résistance après 48h de traitement avec le paraquat comparé à deux autre aptamères peptidiques, Apta-34 et Apta-TRX (sans boucle de contrôle variable). Une autre étude a révélé un défaut dans la phagocytose des corps apoptotiques au cours du développement embryonnaire de la drosophile exprimant Apta-32 dans les macrophages, ce qui suggère qu’Apta-32 pourrait participer à et peut-être interférer avec le processus de l’autophygie, et que Apta-32 pourrait protéger contre l'autophagie induite par paraquat dans les neurones
Parkinson’s disease is considered as the second most common neurodegenerative disease. Although the cause of the progressive cell loss of PD remains unclear to date, programmed cell death, inflammation and autophagy due to oxidative stress, gene mutations or protein aggregations within DA neuron have been suggested as potential causes. Peptide aptamers are small combinatorial proteins, with a variable loop inserted into a scaffold protein, human thioredoxin, hTRX. They are used to facilitate dissection of signaling networks by modulating specific protein interactions and functions. Two peptide aptamers were identified by functional selection which inhibit Bax-dependent cell death in mammalian models. One peptide aptamer (Apta-32) is binding two paralogues involved in endocytotic trafficking T32. The second peptide aptamer (Apta-34) is binding to a target "T34", a pro-apoptotic protein mediating apoptosis emanating from the nucleus. The work of my PhD thesis aimed to investigate the anti-apoptotic function of our two peptide aptamers in different PD models including cell model (in vitro), brain tissue slice and D. melanogaster (in vivo) ; in particular their impact on neuron survival after exposure to specific toxins. Two major toxins were applied in this work, 6-hydroxindopamine (6-OHDA) and Paraquat, a commonly used pesticide. Our observations indicated that Drosophila expressing Apta-32 in all neurons showed more resistance 48h after treatment with Paraquat, compared to drosophila expressing Apta-34 or TRX. Another study revealed a defect in phagocytosis of apoptotic bodies in drosophila embryo’s expressing Apta-32 in macrophage, suggesting Apta-32 could be involved in, and perhaps interfere with, the process of autophagy. This suggests that Apta-32 could protect against paraquat induced autophagy in neurons
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Hobani, Yahya Hasan. "Metabolomic analyses of Drosophila models for human renal disease." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3222/.

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Inborn errors of metabolism (IEMs) constitute a major class of genetic disorder. Most of IEMs are transmitted recessively, so consanguinity has a huge impact on disease prevalence, particularly in societies like Saudi Arabia, where consanguineous marriage is common. Understanding and treatment are very important in genetic diseases, and simple models would be helpful. Thus, the feasibility of applying the fruit fly, Drosophila melanogaster, as a model for a human renal genetic disease - xanthinuria - was investigated. Xanthinuria is a rare human genetic disease, caused by mutations in xanthine oxidase or molybdenum cofactor sulphurase; in Drosophila, the homologous genes are rosy (ry) and maroon-like (mal), respectively. The new Orbitrap technology of mass spectrometry has the potential to determine levels of many metabolites simultaneously by exact mass, and a major part of this thesis was to investigate the utility of Orbitrap technology in metabolomics of both wild-type and Drosophila mutant. Repeatable significant differences were identified between ry and wild-type flies, which recapitulated painstaking analytical biochemical determinations of the 1950s, but with greater precision. Additionally, completely novel impacts of the ry mutation (on pyrimidine metabolism, the urea cycle and osmolyte biosynthesis) were identified. As expected mal mutants showed more similar changes as ry, but with widespread metabolic perturbations. The online resource, FlyAtlas.org, provides detailed microarray-based expression data for multiple tissues and life-stages of Drosophila. Downstream genes, such as urate oxidase, are utterly tubule-specific. Accordingly, the utility of Orbitrap technology in elucidating tissue-specific metabolomes was also investigated. Additionally, genetic interventions using designed RNAi constructs were also made and validated by QPCR and metabolomics. As urate is a potent antioxidant, survival of urate oxidase knockdowns was tested in vivo, and a significant impact on survival identified. An Affymetrix microarray was performed, comparing ry506 mutant flies against wild-type and differences were identified in a second experiment, the anti-gout drug allopurinol was used to phenocopy the effects of ry. Overall, the thesis showed that Orbitrap technology was highly suitable for metabolomic analysis of both wild-type and mutant Drosophila, and had potential in the analysis of metabolomes of single tissues. The possibility of using Orbitrap-based metabolomicsin human diagnosis is discussed.
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Vargas, Miguel. "Nutrient response and aging in invertebrate models." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/nutrient-response-and-aging-in-invertebrate-models(3fccf140-7906-4fad-9892-b8957dc44a04).html.

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The diet an organism keeps is crucial in sustaining its health and fitness. The fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans are excellent models for nutritional studies due to their small size, large progeny numbers, quick development, and modifiable laboratory diets. Here I examine these two organisms in order to better understand the complex interrelationship between an animal and its diet. Previous work has shown that in the wild numerous organisms are capable of selecting specific nutrients in a non-random manner in order to maximize fitness. However, the genetic underpinnings driving these nutrient choices remain elusive. Female fruit flies consume higher levels of protein following mating to prepare for the costs of reproduction. I examined the role of S6 Kinase (S6K), a downstream effector of the nutrient-responsive target of rapamycin pathway, in mediating this decision. I demonstrate that neuronal S6K activity and serotonin are involved in regulating protein consumption when allowed to choose nutrients freely as well as following macronutrient deprivation; suggesting that they may play a role in mediating postmating dietary switch and maintaining nutrient balance. Modulating levels of dietary components can have extensive impacts on processes such as development, fecundity, and metabolism in multiple organisms. However, the influence of dietary genetics on the consumer is virtually unknown. I performed a screen feeding single-gene mutants of E. coli to C. elegans and monitored the effects on the insulin-like signalling pathway (ILS). When mutated, genes involved in multiple processes and functions in E. coli enhanced activity of the ILS downstream transcription factor, DAF-16. One mutant strain of E. coli I pursued had a knockout of the cAMP-producing, adenylate cyclase gene. Addition of exogenous cAMP to the diet containing live, metabolically active E. coli rescued all the effects of the mutant on C. elegans; thereby suggesting that bacterial metabolism of dietary cAMP can influence the C. elegans ILS. Collectively, my work demonstrates how the nutrient-sensing pathways of the consumer can shape and be shaped by interactions with its diet. These studies contribute to a better understanding of the consumer-diet relationship, and could help guide future work to investigate the role of diet in disease, quality of life, and longevity.
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Snigdha, Kirti. "Study of Tumor Development Using Drosophila melanogaster Models." University of Dayton / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=dayton1591210557481631.

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Xun, Zhiyin. "Understanding Parkinson's disease through proteome analyses of Drosophila melanogaster models." [Bloomington, Ind.] : Indiana University, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3344612.

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Thesis (Ph. D.)--Indiana University, Dept. of Chemistry, 2008.
Title from PDF t.p. (viewed Oct. 7, 2009). Source: Dissertation Abstracts International, Volume: 70-02, Section: B, page: 0993. Adviser: David E. Clemmer. Includes supplementary digital materials.
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Michel, Claire Hélène Marie. "Investigating inflammation in a Drosophila model of Alzheimer's disease." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608998.

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Girard, Victor. "Understanding lipid droplet biogenesis in the central nervous system of Drosophila models of Parkinson's disease." Thesis, Lyon, 2020. http://www.theses.fr/2020LYSEN083.

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Les maladies neurodégénératives sont l’une des principales causes d’invalidité dans le monde. Certaines de ces maladies, telle que la maladie de Parkinson (MP), sont associées à des dérégulations du métabolisme lipidique. En effet, plusieurs laboratoires dont le nôtre, ont montré que l’accumulation d’acide gras sous forme de gouttelettes lipidiques (GLs) dans les cellules gliales est un mécanisme de réponse au stress oxydatif conservé au cours de l’évolution. De plus, la formation de GLs dans les neurones pourrait aussi participer au processus neurodégénératif. La contribution respective des cellules gliales et des neurones reste cependant peu étudiée. Au cours de ma thèse, je me suis intéressé aux mécanismes et conséquences pathologiques de l’accumulation de GLs dans les neurones et les cellules gliales. La MP est caractérisée par l’accumulation d’alpha-synucléine (aSyn) sous forme d’agrégats intracellulaires appelés corps de Lewy. L’aSyn est une protéine normalement localisée aux synapses contenant un domaine de liaison aux lipides. L’aSyn peut se lier à la surface des GLs in vitro et l’expression d’aSyn humaine dans la levure induit l’accumulation de GLs. Cependant, la conservation et relevance de ce processus dans le cadre de la MP restent à démontrer. Durant ma thèse, j’ai montré que l’expression simultanée de l’aSyn et de périlipine, une protéine de surface des GLs, induit l’accumulation de GLs dans les neurones photorécepteurs de la rétine de drosophile. De plus, l’aSyn se localise à la surface des GLs dans les photorécepteurs de drosophiles et les neuroblastes humains en culture. Mes résultats suggèrent que l’association de l’aSyn et des périlipines aux GLs, pourrait les stabiliser et favoriser leur accumulation. Enfin, la présence de GLs dans les photorécepteurs augmente la résistance de l’aSyn à la digestion par protéinase K, suggérant que les GLs sont impliquées dans la conversion pathologique de l’aSyn vers des formes agrégées.Les cellules gliales maintiennent l’intégrité du système nerveux central et peuvent accumuler des GLs en réponse à des dommages neuronal ou du stress. J’ai montré que Split-ends (Spen), une protéine identifiée comme facteur de survie des cellules gliales au cours du développement, est impliquée dans le maintien de l’homéostasie des GLs dans les cellules gliales de drosophile adulte. De plus, l’expression de spen promeut la résistance des mouches au traitement par le Paraquat, un pesticide reconnu comme facteur de risque pour la MP chez l’homme. Ces résultats suggèrent que les fonctions de spen dans le maintien de l’homéostasie lipidique dans les cellules gliales protègent contre le stress oxydatif induit par le paraquat.Collectivement, les résultats obtenus au cours de ma thèse montrent que le maintien de l’homéostasie des GLs dans les cellules gliales mais également dans les neurones est important dans les processus pathologiques associés à la MP
Neurodegenerative disorders are a worldwide leading cause of disability. Several neurodegenerative disorders including Parkinson's disease (PD) are associated with lipid storage dysregulation in the brain. In particular, the storage of lipids in cytoplasmic organelles, called lipid droplets (LDs), has recently emerged as important mechanism of the stress response. Several labs including ours, found that LD accumulation in glia may promote neuronal survival in condition of oxidative stress. Interestingly, in the context of neurodegeneration, neurons can also accumulate LDs. The contribution of neuronal and glial cells LDs to neurodegeneration remains a topic of debate. During my PhD, I investigated the mechanisms and consequences of LD accumulation in neurons and glia in two Drosophila models of PD. PD is characterized by the accumulation of misfolded alpha-synuclein (aSyn) in neuronal cytoplasmic inclusions. Interestingly, aSyn contains a lipid-binding domain that shares structural similarities with LD-binding proteins such as perilipins and aSyn can bind synthetic LD in vitro and induces LD accumulation in yeast by a mechanism that remains unclear. I found that expression of aSyn in association with perilipin impairs LD homeostasis leading to accumulation of LDs in Drosophila photoreceptor neurons. Interestingly, I observed that aSyn co-localizes with perilipins on LD surface in both Drosophila photoreceptor neurons and human neuroblastoma cells. I thus proposed that aSyn by associating with perilipins stabilize LD and by this mean promote LD accumulation. Finally, modulating LD content in photoreceptor impacts aSyn resistance to proteinase K suggesting that LDs are involved in pathological conversion of aSyn. Glial cells are early sensor of central nervous system injuries that accumulate LDs in response to neuronal stress to protect neurons from damages associated with lipid peroxidation. We found that Split-ends (Spen), an RNA binding protein previously identified as a glial pro-survival factor during development, maintains LD homeostasis in adult glial cell. In addition, expression of spen was associated with resistance to paraquat-induced neurotoxicity, a pesticide associated with increased risk of PD in human epidemiologic studies. These results suggest that Spen-mediated lipid metabolism functions is important for neuroprotection in PD.Collectively the results of my thesis provide new evidences for the formation of LDs in both neurons and glial cells and their contribution in the progression of PD pathology
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Ferlito, Valentina Claudia. "Evaluating the potential for neurodegenerative disease models in juvenile Drosophila melanogaster." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28834.

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With 9.9 million new dementia cases each year, Alzheimer’s and Parkinson’s disease (AD and PD) are the most prevalent form of neurodegenerative disorder (NDG) affecting the aging population. Despite years of pharmaceutical research, no cure is yet available. Most neuropathological aspects of these diseases are extremely complex but the study of the rare genetic cases allowed to model these diseases in animals and uncover key pathophysiological processes. Transgenic Drosophila NDG models have been used for in vivo studies for many years with a range of relevant phenotypes. The cellular and molecular biology of the Central Nervous System, as well as the mechanisms underlying neurodegeneration, are well conserved between Drosophila and Humans (with a 75% of human disease-related genes having homologs in flies). Most NDG studies are performed in the aging flies. However, there are reports of measurable phenotypes for a variety of AD and PD models in juvenile Drosophila melanogaster (larval stage) with an unexploited considerable potential for drug discovery and screening for this outstanding model. Here I sought to develop a new assay for research into NDGs that focus on the earliest phenotypes. During this Ph.D. project a customized crawling assay apparatus was developed, for the assessment of locomotor ability in humanised larval Drosophila (overexpressing human proteins/peptides linked to AD and PD). A locomotor phenotype was identified in larvae overexpressing different variation of Amyloid-β42, tau and α-Synuclein pan neutrally: these animals crawl on agarose surface at a reduced mean speed when compared to controls. The defect was proven partially rescuable by administration of Tacrine and Methylene Blue, renewing the importance of such models for future applications in drug discovery and screening. The motor impairment supports the hypothesis of a neurotoxic effect of the protein/peptide. Thus, to test this further, the overexpression of the human transgenes was restricted to neurons involved in larval olfaction (olfactory impairment is often the earliest symptom in PD and AD) and odour associated learning tasks (both PD and AD are characterized by severe cognitive dysfunction). Interestingly, larvae overexpressing the Amyloid-β42 ARC peptide in the Olfactory Sensory Neurons showed a subtle navigation defect during chemotaxis (in 1-Hexanol odour gradient) that could possibly be addressed to premature neural habituation to the olfactory stimulus. Furthermore, the overexpression of the peptide in the larval Mushroom Bodies influenced the performances of the animals in associative learning tasks. Lastly, using immunohistochemistry and confocal imaging techniques I showed that the gross morphology of neurons is not altered by the targeted overexpression of the Amyloid-β42 ARC. Even though physiological studies are required to characterize the chemosensory/learning defect shown by the Amyloid-β42 ARC larvae, this Ph.D. work further confirms that the effects of the overexpression of the human transgenes are robust and measurable already at larval stage. These findings may also be relevant to the development of new, fast, and cost-effective compound screening procedures, for applications in early stages of the drug discovery process.
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Page, Richard Mark Donald. "Pathways of amyloid-β neurotoxicity in a Drosophila model of Alzheimer's disease." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612858.

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MacLeod, Ian. "A Drosophila model of familial encephalopathy with neuroserpin inclusion bodies." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611439.

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Books on the topic "Drosophila models"

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Yamaguchi, Masamitsu, ed. Drosophila Models for Human Diseases. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-0529-0.

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Progress and prospects in evolutionary biology: The Drosophila model. New York: Oxford University Press, 1997.

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Budnik, Vivian. The fly neuromuscular junction: Structure and function. 2nd ed. San Diego, Calif: Elsevier/Academic Press, 2006.

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Vivian, Budnik, and Ruiz-Cãnada Catalina, eds. The Fly neuromuscular junction: Structure and function. 2nd ed. San Diego, Calif: Elsevier/Academic Press, 2006.

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Deng, Wu-Min, ed. The Drosophila Model in Cancer. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-23629-8.

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Lints, Frédéric A., and M. Hani Soliman, eds. Drosophila as a Model Organism for Ageing Studies. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2683-8.

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Drosophila. Humana Press, 2008.

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Yamaguchi, Masamitsu. Drosophila Models for Human Diseases. Springer, 2018.

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Yamaguchi, Masamitsu. Drosophila Models for Human Diseases. Springer, 2020.

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Yamaguchi, Masamitsu. Drosophila Models for Human Diseases. Springer, 2019.

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Book chapters on the topic "Drosophila models"

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Sander, Moritz, and Héctor Herranz. "MicroRNAs in Drosophila Cancer Models." In Advances in Experimental Medicine and Biology, 157–73. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-23629-8_9.

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Myers, Ryan R., and Pedro Fernandez-Funez. "Drosophila Models of Prion Diseases." In Prions and Diseases, 313–49. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-20565-1_17.

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Androschuk, Alaura, and Francois V. Bolduc. "Modeling Intellectual Disability in Drosophila." In Animal Models of Neurodevelopmental Disorders, 215–37. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2709-8_14.

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Kim, Yong-Kyu. "A Drosophila Model for Aggression." In Animal Models of Behavior Genetics, 35–61. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3777-6_2.

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Yamaguchi, Masamitsu, and Hiroshi Takashima. "Drosophila Charcot-Marie-Tooth Disease Models." In Advances in Experimental Medicine and Biology, 97–117. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-0529-0_7.

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Hyde, David R., Scott Milligan, and Troy Zars. "Rhodopsin-Dependent Models of Drosophila Photoreceptor Degeneration." In Degenerative Retinal Diseases, 145–58. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5933-7_18.

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Szabo, Aron, and George K. Tofaris. "Monitoring α-Synuclein Proteotoxicity in Drosophila Models." In Methods in Molecular Biology, 199–208. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9124-2_15.

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Brace, E. J., and Aaron DiAntonio. "Models of Axon Degeneration in Drosophila Larvae." In Methods in Molecular Biology, 311–20. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0585-1_23.

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Sujkowski, Alyson, and Robert Wessells. "Drosophila Models of Cardiac Aging and Disease." In Life Extension, 127–50. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18326-8_6.

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Song, Juan, and Mark A. Tanouye. "The Genetics and Molecular Biology of Seizure Susceptibility in Drosophila." In Animal Models of Epilepsy, 27–43. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-263-6_2.

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Conference papers on the topic "Drosophila models"

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Wu, Penghe, Airong Li, Jing Men, Rudolph E. Tans, and Chao Zhou. "Optogenetic pacing in Drosophila models (Conference Presentation)." In Diagnosis and Treatment of Diseases in the Breast and Reproductive System III, edited by Melissa C. Skala and Paul J. Campagnola. SPIE, 2017. http://dx.doi.org/10.1117/12.2251653.

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Carter, John, Jocelyn Rego, Daniel Schwartz, Vikas Bhandawat, and Edward Kim. "Learning Spiking Neural Network Models of Drosophila Olfaction." In ICONS 2020: International Conference on Neuromorphic Systems 2020. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3407197.3407214.

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Koppes, Ryan A., Douglas M. Swank, and David T. Corr. "Force Depression in the Drosophila Jump Muscle." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19436.

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The depression of isometric force after active shortening, termed force depression (FD), is a well-accepted characteristic of skeletal muscle that has been demonstrated in both whole muscle [1,3] and single-fiber preparations [1,2]. Although this history-dependent behavior has been observed experimentally for over 70 years, its underlying mechanism(s) remain unknown. Drosophila melangastor, commonly known as the fruit fly, is a well established, comprehensively understood, and genetically manipulable animal model. Furthermore, Drosophila have proved to be an accurate model species for studying muscle mechanics, and the Tergal Depressor of the Trochanter (TDT), or jump muscle, has most precisely resembled the mechanics of mammalian skeletal muscle [4]. Due to the structural and phenomenological similarities of the TDT muscle to skeletal muscle, in addition to the potential use of genetic mutations in fly models, it is extremely advantageous to investigate the presence of history dependent phenomenon in the TDT. If such phenomena are present, further investigation utilizing different myosin and actin isoforms to study the underlying mechanism(s) could produce new insight into this history-dependent phenomenon, otherwise impossible to elucidate using current experimental models. Thus, it is the goal of this study to determine the presence and degree of FD in the TDT muscle of wild type Drosophila.
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Razetti, A., X. Descombes, C. Medioni, and F. Besse. "Statistical Characterization, Modelling and Classification of Morphological Changes in imp Mutant Drosophila Gamma Neurons." In 7th International Conference on Bioinformatics Models, Methods and Algorithms. SCITEPRESS - Science and and Technology Publications, 2016. http://dx.doi.org/10.5220/0005703800630074.

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Levinson, Sarah, and Ross Cagan. "Abstract 5150: Drosophila models of Ret fusions in papillary thyroid carcinoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5150.

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Gopinath, Sindhura, Ross Cagan, and Eric Schadt. "Abstract B17: Modeling genomic complexity of colorectal cancer using multigenic Drosophila models." In Abstracts: AACR Special Conference on the Evolving Landscape of Cancer Modeling; March 2-5, 2020; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.camodels2020-b17.

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"Analysis of robust pattern formation in the developing Drosophila eye using two mathematical models." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-395.

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Sadler, Freja, Thomas Massey, Gaynor Smith, and Lesley Jones. "A01 Investigating the effect of dna maintenance genes in drosophila melanogaster models of huntington’s disease." In EHDN Abstracts 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jnnp-2021-ehdn.1.

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Bangi, Erdem, Claudio Murgia, Alexander Teague, Owen Sansom, and Ross Cagan. "Abstract PR03: Identifying biomarkers of drug response and resistance using personalized Drosophila models of colorectal cancer." In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-pr03.

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Vasquez Jaramillo, Juan David, Mauricio A. Alvarez, and Alvaro A. Orozco. "Latent force models for describing transcriptional regulation processes in the embryo development problem for the Drosophila melanogaster." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6943598.

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Reports on the topic "Drosophila models"

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Walker, James A. Developing a Drosophila Model of Schwannomatosis. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada575950.

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Walker, James A. Developing a Drosophila Model of Schwannomatosis. Fort Belvoir, VA: Defense Technical Information Center, February 2013. http://dx.doi.org/10.21236/ada575951.

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Weilbaecher, Katherine, and Ross Cagan. Assessing a Drosophila Metastasis Model in Mouse and Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2008. http://dx.doi.org/10.21236/ada488819.

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Weilbaecher, Katherine, and Ross Cagan. Assessing a Drosophila Metastasis Model in Mouse and Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2009. http://dx.doi.org/10.21236/ada625288.

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Ito, Naoto. A Novel Locomotion-based Validation Assay for Candidate Drugs Using Drosophila DYT1 Disease Model. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada608248.

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Ito, Naoto. A Novel Locomotion-based Validation Assay for Candidate Drugs Using Drosophila DYT1 Disease Model. Fort Belvoir, VA: Defense Technical Information Center, November 2013. http://dx.doi.org/10.21236/ada595245.

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Ohad, Nir, and Robert Fischer. Control of Fertilization-Independent Development by the FIE1 Gene. United States Department of Agriculture, August 2000. http://dx.doi.org/10.32747/2000.7575290.bard.

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A fundamental problem in biology is to understand how fertilization initiates reproductive development. During plant reproduction, one sperm cell fuses with the egg to form an embryo, whereas a second sperm cell fuses with the adjacent central cell nucleus to form the endosperm tissue that supports embryo and/or seedling development. To understand the mechanisms that initiate reproduction, we have isolated mutants of Arabidopsis that allow for replication of the central cell and subsequent endosperm development without fertilization. In this project we have cloned the MEA gene and showed that it encode a SET- domain polycomb protein. Such proteins are known to form chromatin-protein complexes that repress homeotic gene transcription and influence cell proliferation from Drosophylla to mammals. We propose a model whereby MEA and an additional polycomb protein we have cloned, FIE , function to suppress a critical aspect of early plant reproduction and endosperm development, until fertilization occurs. Using a molecular approach we were able to determine that FIE and MEA interact physically, suggesting that these proteins have been conserved also during the evolution of flowering plants. The analysis of MEA expression pattern revealed that it is an imprinted gene that displays parent-of- origin-dependent monoallelic expression specifically in the endosperm tissue. Silencing of the paternal MEA allele in the endosperm and the phenotype of mutant mea seeds support the parental conflict theory for the evolution of imprinting in plants and mammals. These results contribute new information on the initiation of endosperm development and provide a unique entry point to study asexual reproduction and apomixis which is expected to improve crop production.
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Rafaeli, Ada, Russell Jurenka, and Daniel Segal. Isolation, Purification and Sequence Determination of Pheromonotropic-Receptors. United States Department of Agriculture, July 2003. http://dx.doi.org/10.32747/2003.7695850.bard.

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Moths constitute a major group of pest insects in agriculture. Pheromone blends are utilised by a variety of moth species to attract conspecific mates, which is under circadian control by the neurohormone, PBAN (pheromone-biosynthesis-activating neuropeptide). Our working hypothesis was that, since the emission of sex-pheromone is necessary to attract a mate, then failure to produce and emit pheromone is a potential strategy for manipulating adult moth behavior. The project aimed at identifying, characterising and determining the sequence of specific receptors responsible for the interaction with pheromonotropic neuropeptide/s using two related moth species: Helicoverpa armigera and H. lea as model insects. We established specific binding to a membrane protein estimated at 50 kDa in mature adult females using a photoaffinity-biotin probe for PBAN. We showed that JH is required for the up-regulation of this putative receptor protein. In vitro studies established that the binding initiates a cascade of second messengers including channel opening for calcium ions and intracellular cAMP production. Pharmacological studies (using sodium fluoride) established that the receptor is coupled to a G-protein, that is, the pheromone-biosynthesis-activating neuropeptide receptor (PBAN-R) belongs to the family of G protein-coupled receptor (GPCR)'s. We showed that PBAN-like peptides are present in Drosophila melanogaster based on bioassay and immunocytochemical data. Using the annotated genome of D. melanogaster to search for a GPCR, we found that some were similar to neuromedin U- receptors of vertebrates, which contain a similar C-terminal ending as PBAN. We established that neuromedin U does indeed induce pheromone biosynthesis and cAMP production. Using a PCR based cloning strategy and mRNA isolated from pheromone glands of H. zea, we successfully identified a gene encoding a GPCR from pheromone glands. The full-length PBAN-R was subsequently cloned and expressed in Sf9 insect cells and was shown to mobilize calcium in response to PBAN in a dose-dependent manner. The successful progress in the identification of a gene, encoding a GPCR for the neurohormone, PBAN, provides a basis for the design of a novel battery of compounds that will specifically antagonize pheromone production. Furthermore, since PBAN belongs to a family of insect neuropeptides with more than one function in different life stages, this rationale may be extended to other physiological key-regulatory processes in different insects.
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Rafaeli, Ada, Russell Jurenka, and Chris Sander. Molecular characterisation of PBAN-receptors: a basis for the development and screening of antagonists against Pheromone biosynthesis in moth pest species. United States Department of Agriculture, January 2008. http://dx.doi.org/10.32747/2008.7695862.bard.

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The original objectives of the approved proposal included: (a) The determination of species- and tissue-specificity of the PBAN-R; (b) the elucidation of the role of juvenile hormone in gene regulation of the PBAN-R; (c) the identificationof the ligand binding domains in the PBAN-R and (d) the development of efficient screening assays in order to screen potential antagonists that will block the PBAN-R. Background to the topic: Moths constitute one of the major groups of pest insects in agriculture and their reproductive behavior is dependent on chemical communication. Sex-pheromone blends are utilised by a variety of moth species to attract conspecific mates. In most of the moth species sex-pheromone biosynthesis is under circadian control by the neurohormone, PBAN (pheromone-biosynthesis-activating neuropeptide). In order to devise ideal strategies for mating disruption/prevention, we proposed to study the interactions between PBAN and its membrane-bound receptor in order to devise potential antagonists. Major conclusions: Within the framework of the planned objectives we have confirmed the similarities between the two Helicoverpa species: armigera and zea. Receptor sequences of the two Helicoverpa spp. are 98% identical with most changes taking place in the C-terminal. Our findings indicate that PBAN or PBAN-like receptors are also present in the neural tissues and may represent a neurotransmitter-like function for PBAN-like peptides. Surprisingly the gene encoding the PBAN-receptor was also present in the male homologous tissue, but it is absent at the protein level. The presence of the receptor (at the gene- and protein-levels), and the subsequent pheromonotropic activity are age-dependent and up-regulated by Juvenile Hormone in pharate females but down-regulated by Juvenile Hormone in adult females. Lower levels of pheromonotropic activity were observed when challenged with pyrokinin-like peptides than with HezPBAN as ligand. A model of the 3D structure of the receptor was created using the X-ray structure of rhodopsin as a template after sequence alignment of the HezPBAN-R with several other GPCRs and computer simulated docking with the model predicted putative binding sites. Using in silico mutagenesis the predicted docking model was validated with experimental data obtained from expressed chimera receptors in Sf9 cells created by exchanging between the three extracellular loops of the HezPBAN-R and the Drosophila Pyrokinin-R (CG9918). The chimera receptors also indicated that the 3ʳᵈ extracellular loop is important for recognition of PBAN or Diapause hormone ligands. Implications: The project has successfully completed all the objectives and we are now in a position to be able to design and screen potential antagonists for pheromone production. The successful docking simulation-experiments encourage the use of in silico experiments for initial (high-throughput) screening of potential antagonists. However, the differential responses between the expressed receptor (Sf9 cells) and the endogenous receptor (pheromone glands) emphasize the importance of assaying lead compounds using several alternative bioassays (at the cellular, tissue and organism levels). The surprising discovery of the presence of the gene encoding the PBAN-R in the male homologous tissue, but its absence at the protein level, launches opportunities for studying molecular regulation pathways and the evolution of these GPCRs. Overall this research will advance research towards the goal of finding antagonists for this important class of receptors that might encompass a variety of essential insect functions.
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Altstein, Miriam, and Ronald J. Nachman. Rational Design of Insect Control Agent Prototypes Based on Pyrokinin/PBAN Neuropeptide Antagonists. United States Department of Agriculture, August 2013. http://dx.doi.org/10.32747/2013.7593398.bard.

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The general objective of this study was to develop rationally designed mimetic antagonists (and agonists) of the PK/PBAN Np class with enhanced bio-stability and bioavailability as prototypes for effective and environmentally friendly pest insect management agents. The PK/PBAN family is a multifunctional group of Nps that mediates key functions in insects (sex pheromone biosynthesis, cuticular melanization, myotropic activity, diapause and pupal development) and is, therefore, of high scientific and applied interest. The objectives of the current study were: (i) to identify an antagonist biophores (ii) to develop an arsenal of amphiphilic topically active PK/PBAN antagonists with an array of different time-release profiles based on the previously developed prototype analog; (iii) to develop rationally designed non-peptide SMLs based on the antagonist biophore determined in (i) and evaluate them in cloned receptor microplate binding assays and by pheromonotropic, melanotropic and pupariation in vivo assays. (iv) to clone PK/PBAN receptors (PK/PBAN-Rs) for further understanding of receptor-ligand interactions; (v) to develop microplate binding assays for screening the above SMLs. In the course of the granting period A series of amphiphilic PK/PBAN analogs based on a linear lead antagonist from the previous BARD grant was synthesized that incorporated a diverse array of hydrophobic groups (HR-Suc-A[dF]PRLa). Others were synthesized via the attachment of polyethylene glycol (PEG) polymers. A hydrophobic, biostablePK/PBAN/DH analog DH-2Abf-K prevented the onset of the protective state of diapause in H. zea pupae [EC50=7 pmol/larva] following injection into the preceding larval stage. It effectively induces the crop pest to commit a form of ‘ecological suicide’. Evaluation of a set of amphiphilic PK analogs with a diverse array of hydrophobic groups of the formula HR-Suc-FTPRLa led to the identification of analog T-63 (HR=Decyl) that increased the extent of diapause termination by a factor of 70% when applied topically to newly emerged pupae. Another biostablePK analog PK-Oic-1 featured anti-feedant and aphicidal properties that matched the potency of some commercial aphicides. Native PK showed no significant activity. The aphicidal effects were blocked by a new PEGylated PK antagonist analog PK-dF-PEG4, suggesting that the activity is mediated by a PK/PBAN receptor and therefore indicative of a novel and selective mode-of-action. Using a novel transPro mimetic motif (dihydroimidazole; ‘Jones’) developed in previous BARD-sponsored work, the first antagonist for the diapause hormone (DH), DH-Jo, was developed and shown to block over 50% of H. zea pupal diapause termination activity of native DH. This novel antagonist development strategy may be applicable to other invertebrate and vertebrate hormones that feature a transPro in the active core. The research identifies a critical component of the antagonist biophore for this PK/PBAN receptor subtype, i.e. a trans-oriented Pro. Additional work led to the molecular cloning and functional characterization of the DH receptor from H. zea, allowing for the discovery of three other DH antagonist analogs: Drosophila ETH, a β-AA analog, and a dF analog. The receptor experiments identified an agonist (DH-2Abf-dA) with a maximal response greater than native DH. ‘Deconvolution’ of a rationally-designed nonpeptide heterocyclic combinatorial library with a cyclic bis-guanidino (BG) scaffold led to discovery of several members that elicited activity in a pupariation acceleration assay, and one that also showed activity in an H. zea diapause termination assay, eliciting a maximal response of 90%. Molecular cloning and functional characterization of a CAP2b antidiuretic receptor from the kissing bug (R. prolixus) as well as the first CAP2b and PK receptors from a tick was also achieved. Notably, the PK/PBAN-like receptor from the cattle fever tick is unique among known PK/PBAN and CAP2b receptors in that it can interact with both ligand types, providing further evidence for an evolutionary relationship between these two NP families. In the course of the granting period we also managed to clone the PK/PBAN-R of H. peltigera, to express it and the S. littoralis-R Sf-9 cells and to evaluate their interaction with a variety of PK/PBAN ligands. In addition, three functional microplate assays in a HTS format have been developed: a cell-membrane competitive ligand binding assay; a Ca flux assay and a whole cell cAMP ELISA. The Ca flux assay has been used for receptor characterization due to its extremely high sensitivity. Computer homology studies were carried out to predict both receptor’s SAR and based on this analysis 8 mutants have been generated. The bioavailability of small linear antagonistic peptides has been evaluated and was found to be highly effective as sex pheromone biosynthesis inhibitors. The activity of 11 new amphiphilic analogs has also been evaluated. Unfortunately, due to a problem with the Heliothis moth colony we were unable to select those with pheromonotropic antagonistic activity and further check their bioavailability. Six peptides exhibited some melanotropic antagonistic activity but due to the low inhibitory effect the peptides were not further tested for bioavailability in S. littoralis larvae. Despite the fact that no new antagonistic peptides were discovered in the course of this granting period the results contribute to a better understanding of the interaction of the PK/PBAN family of Nps with their receptors, provided several HT assays for screening of libraries of various origin for presence of PK/PBAN-Ragonists and antagonists and provided important practical information for the further design of new, peptide-based insecticide prototypes aimed at the disruption of key neuroendocrine physiological functions in pest insects.
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