Статті в журналах: "Drosophila models"

1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

J. Murray, Michael. "Drosophila models of metastasis." AIMS Genetics 2, no. 1 (2015): 25–53. http://dx.doi.org/10.3934/genet.2015.1.25.

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12

E. Richardson, Helena. "Drosophila models of cancer." AIMS Genetics 2, no. 1 (2015): 97–103. http://dx.doi.org/10.3934/genet.2015.1.97.

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13

Jeon, Youngjae, Jae Ha Lee, Byoungyun Choi, So-Yoon Won, and Kyoung Sang Cho. "Genetic Dissection of Alzheimer’s Disease Using Drosophila Models." International Journal of Molecular Sciences 21, no. 3 (January 30, 2020): 884. http://dx.doi.org/10.3390/ijms21030884.

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Alzheimer’s disease (AD), a main cause of dementia, is the most common neurodegenerative disease that is related to abnormal accumulation of the amyloid β (Aβ) protein. Despite decades of intensive research, the mechanisms underlying AD remain elusive, and the only available treatment remains symptomatic. Molecular understanding of the pathogenesis and progression of AD is necessary to develop disease-modifying treatment. Drosophila, as the most advanced genetic model, has been used to explore the molecular mechanisms of AD in the last few decades. Here, we introduce Drosophila AD models based on human Aβ and summarize the results of their genetic dissection. We also discuss the utility of functional genomics using the Drosophila system in the search for AD-associated molecular mechanisms in the post-genomic era.

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14

Szikora, Szilárd, Péter Görög, Csaba Kozma, and József Mihály. "Drosophila Models Rediscovered with Super-Resolution Microscopy." Cells 10, no. 8 (July 29, 2021): 1924. http://dx.doi.org/10.3390/cells10081924.

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With the advent of super-resolution microscopy, we gained a powerful toolbox to bridge the gap between the cellular- and molecular-level analysis of living organisms. Although nanoscopy is broadly applicable, classical model organisms, such as fruit flies, worms and mice, remained the leading subjects because combining the strength of sophisticated genetics, biochemistry and electrophysiology with the unparalleled resolution provided by super-resolution imaging appears as one of the most efficient approaches to understanding the basic cell biological questions and the molecular complexity of life. Here, we summarize the major nanoscopic techniques and illustrate how these approaches were used in Drosophila model systems to revisit a series of well-known cell biological phenomena. These investigations clearly demonstrate that instead of simply achieving an improvement in image quality, nanoscopy goes far beyond with its immense potential to discover novel structural and mechanistic aspects. With the examples of synaptic active zones, centrosomes and sarcomeres, we will explain the instrumental role of super-resolution imaging pioneered in Drosophila in understanding fundamental subcellular constituents.

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15

Cowan, Catherine M., David Shepherd, and Amritpal Mudher. "Insights from Drosophila models of Alzheimer's disease." Biochemical Society Transactions 38, no. 4 (July 26, 2010): 988–92. http://dx.doi.org/10.1042/bst0380988.

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AD (Alzheimer's disease) is a neurodegenerative disorder characterized by the abnormal hyperphosphorylation and aggregation of the microtubule-associated protein tau and the misfolding and deposition of Aβ peptide. The mechanisms by which tau and Aβ become abnormal is not clearly understood, neither is it known what role either protein plays in the neurodegenerative process underlying AD. We have modelled aspects of AD in Drosophila melanogaster to shed light on these processes and to further our understanding of the relationship between tau and amyloid in this disease.

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16

Moloney, Aileen, David B. Sattelle, David A. Lomas, and Damian C. Crowther. "Alzheimer's disease: insights from Drosophila melanogaster models." Trends in Biochemical Sciences 35, no. 4 (April 2010): 228–35. http://dx.doi.org/10.1016/j.tibs.2009.11.004.

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17

Pereanu, Wayne, and Volker Hartenstein. "Digital three-dimensional models of Drosophila development." Current Opinion in Genetics & Development 14, no. 4 (August 2004): 382–91. http://dx.doi.org/10.1016/j.gde.2004.06.010.

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18

Le, Viet, Edward Anderson, Takuya Akiyama, and Kristi A. Wharton. "Drosophila models of FOP provide mechanistic insight." Bone 109 (April 2018): 192–200. http://dx.doi.org/10.1016/j.bone.2017.11.001.

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19

Lloyd, Thomas E., and J. Paul Taylor. "Flightless flies: Drosophila models of neuromuscular disease." Annals of the New York Academy of Sciences 1184, no. 1 (January 2010): E1—E20. http://dx.doi.org/10.1111/j.1749-6632.2010.05432.x.

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20

Chen, Zhe, Fan Zhang, and Hong Xu. "Human mitochondrial DNA diseases and Drosophila models." Journal of Genetics and Genomics 46, no. 4 (April 2019): 201–12. http://dx.doi.org/10.1016/j.jgg.2019.03.009.

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21

Arefin, Badrul, Martin Kunc, Robert Krautz, and Ulrich Theopold. "The Immune Phenotype of Three Drosophila Leukemia Models." G3 Genes|Genomes|Genetics 7, no. 7 (July 1, 2017): 2139–49. http://dx.doi.org/10.1534/g3.117.039487.

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Abstract Many leukemia patients suffer from dysregulation of their immune system, making them more susceptible to infections and leading to general weakening (cachexia). Both adaptive and innate immunity are affected. The fruit fly Drosophila melanogaster has an innate immune system, including cells of the myeloid lineage (hemocytes). To study Drosophila immunity and physiology during leukemia, we established three models by driving expression of a dominant-active version of the Ras oncogene (RasV12) alone or combined with knockdowns of tumor suppressors in Drosophila hemocytes. Our results show that phagocytosis, hemocyte migration to wound sites, wound sealing, and survival upon bacterial infection of leukemic lines are similar to wild type. We find that in all leukemic models the two major immune pathways (Toll and Imd) are dysregulated. Toll–dependent signaling is activated to comparable extents as after wounding wild-type larvae, leading to a proinflammatory status. In contrast, Imd signaling is suppressed. Finally, we notice that adult tissue formation is blocked and degradation of cell masses during metamorphosis of leukemic lines, which is akin to the state of cancer-dependent cachexia. To further analyze the immune competence of leukemic lines, we used a natural infection model that involves insect-pathogenic nematodes. We identified two leukemic lines that were sensitive to nematode infections. Further characterization demonstrates that despite the absence of behavioral abnormalities at the larval stage, leukemic larvae show reduced locomotion in the presence of nematodes. Taken together, this work establishes new Drosophila models to study the physiological, immunological, and behavioral consequences of various forms of leukemia.

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22

Green, Edward W., and Flaviano Giorgini. "Choosing and using Drosophila models to characterize modifiers of Huntington's disease." Biochemical Society Transactions 40, no. 4 (July 20, 2012): 739–45. http://dx.doi.org/10.1042/bst20120072.

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HD (Huntington's disease) is a fatal inherited gain-of-function disorder caused by a polyQ (polyglutamine) expansion in the htt (huntingtin protein). Expression of mutant htt in model organisms is sufficient to recapitulate many of the cellular defects found in HD patients. Many groups have independently developed Drosophila models of HD, taking advantage of its rapid life cycle, carefully annotated genome and well-established molecular toolkits. Furthermore, unlike simpler models, Drosophila have a complex nervous system, displaying a range of carefully co-ordinated behaviours which offer an exquisitely sensitive readout of neuronal disruption. Measuring HD-associated changes in behaviour in Drosophila therefore offers a window into the earliest stages of HD, when therapeutic interventions might be particularly effective. The present review describes a number of recently developed Drosophila models of HD and offers practical guidance on the advantages and disadvantages of various experimental approaches that can be used to screen these models for modifiers of mutant htt-mediated toxicity.

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23

Carillo, Maria Rosaria, Carla Bertapelle, Filippo Scialò, Mario Siervo, Gianrico Spagnuolo, Michele Simeone, Gianfranco Peluso, and Filomena Anna Digilio. "L-Carnitine in Drosophila: A Review." Antioxidants 9, no. 12 (December 21, 2020): 1310. http://dx.doi.org/10.3390/antiox9121310.

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L-Carnitine is an amino acid derivative that plays a key role in the metabolism of fatty acids, including the shuttling of long-chain fatty acyl CoA to fuel mitochondrial β-oxidation. In addition, L-carnitine reduces oxidative damage and plays an essential role in the maintenance of cellular energy homeostasis. L-carnitine also plays an essential role in the control of cerebral functions, and the aberrant regulation of genes involved in carnitine biosynthesis and mitochondrial carnitine transport in Drosophila models has been linked to neurodegeneration. Drosophila models of neurodegenerative diseases provide a powerful platform to both unravel the molecular pathways that contribute to neurodegeneration and identify potential therapeutic targets. Drosophila can biosynthesize L-carnitine, and its carnitine transport system is similar to the human transport system; moreover, evidence from a defective Drosophila mutant for one of the carnitine shuttle genes supports the hypothesis of the occurrence of β-oxidation in glial cells. Hence, Drosophila models could advance the understanding of the links between L-carnitine and the development of neurodegenerative disorders. This review summarizes the current knowledge on L-carnitine in Drosophila and discusses the role of the L-carnitine pathway in fly models of neurodegeneration.

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24

Fort-Aznar, Laura, Chris Ugbode, and Sean T. Sweeney. "Retrovirus reactivation in CHMP2BIntron5 models of frontotemporal dementia." Human Molecular Genetics 29, no. 16 (July 6, 2020): 2637–46. http://dx.doi.org/10.1093/hmg/ddaa142.

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Abstract Frontotemporal dementia (FTD) is the second most prevalent form of pre-senile dementia after Alzheimer’s disease. Amyotrophic lateral sclerosis (ALS) can overlap genetically, pathologically and clinically with FTD indicating the two conditions are ends of a spectrum and may share common pathological mechanisms. FTD–ALS causing mutations are known to be involved in endosomal trafficking and RNA regulation. Using an unbiased genome-wide genetic screen to identify mutations affecting an FTD–ALS-related phenotype in Drosophila caused by CHMP2BIntron5 expression, we have uncovered repressors of retrovirus (RV) activity as modifiers of CHMP2BIntron5 toxicity. We report that neuronal expression of CHMP2BIntron5 causes an increase in the activity of the endogenous Drosophila RV, gypsy, in the nervous system. Genetically blocking Drosophila gypsy activation and pharmacologically inhibiting viral reverse transcriptase activity prevents degenerative phenotypes observed in fly and rat neurons. These findings directly link endosomal dysfunction to RV de-repression in an FTD–ALS model without TDP-43 pathology. These observations may contribute an understanding to previous discoveries of RV activation in ALS affected patients.

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25

Vatashchuk, Myroslava V., Maria M. Bayliak, Viktoria V. Hurza, Kenneth B. Storey, and Volodymyr I. Lushchak. "Metabolic Syndrome: Lessons from Rodent and Drosophila Models." BioMed Research International 2022 (June 22, 2022): 1–13. http://dx.doi.org/10.1155/2022/5850507.

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Overweight and obesity are health conditions tightly related to a number of metabolic complications collectively called “metabolic syndrome” (MetS). Clinical diagnosis of MetS includes the presence of the increased waist circumference or so-called abdominal obesity, reduced high density lipoprotein level, elevated blood pressure, and increased blood glucose and triacylglyceride levels. Different approaches, including diet-induced and genetically induced animal models, have been developed to study MetS pathogenesis and underlying mechanisms. Studies of metabolic disturbances in the fruit fly Drosophila and mammalian models along with humans have demonstrated that fruit flies and small mammalian models like rats and mice have many similarities with humans in basic metabolic functions and share many molecular mechanisms which regulate these metabolic processes. In this paper, we describe diet-induced, chemically and genetically induced animal models of the MetS. The advantages and limitations of rodent and Drosophila models of MetS and obesity are also analyzed.

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Kim, Taejoon, Bokyeong Song, and Im-Soon Lee. "Drosophila Glia: Models for Human Neurodevelopmental and Neurodegenerative Disorders." International Journal of Molecular Sciences 21, no. 14 (July 9, 2020): 4859. http://dx.doi.org/10.3390/ijms21144859.

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Glial cells are key players in the proper formation and maintenance of the nervous system, thus contributing to neuronal health and disease in humans. However, little is known about the molecular pathways that govern glia–neuron communications in the diseased brain. Drosophila provides a useful in vivo model to explore the conserved molecular details of glial cell biology and their contributions to brain function and disease susceptibility. Herein, we review recent studies that explore glial functions in normal neuronal development, along with Drosophila models that seek to identify the pathological implications of glial defects in the context of various central nervous system disorders.

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27

Himmelberg, Marc M., Ryan J. H. West, Christopher J. H. Elliott, and Alex R. Wade. "Abnormal visual gain control and excitotoxicity in early-onset Parkinson’s disease Drosophila models." Journal of Neurophysiology 119, no. 3 (March 1, 2018): 957–70. http://dx.doi.org/10.1152/jn.00681.2017.

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The excitotoxic theory of Parkinson’s disease (PD) hypothesizes that a pathophysiological degeneration of dopaminergic neurons stems from neural hyperactivity at early stages of disease, leading to mitochondrial stress and cell death. Recent research has harnessed the visual system of Drosophila PD models to probe this hypothesis. Here, we investigate whether abnormal visual sensitivity and excitotoxicity occur in early-onset PD (EOPD) Drosophila models DJ-1αΔ 72, DJ-1βΔ 93, and PINK15. We used an electroretinogram to record steady-state visually evoked potentials driven by temporal contrast stimuli. At 1 day of age, all EOPD mutants had a twofold increase in response amplitudes compared with w̄ controls. Furthermore, we found that excitotoxicity occurs in older EOPD models after increased neural activity is triggered by visual stimulation. In an additional analysis, we used a linear discriminant analysis to test whether there were subtle variations in neural gain control that could be used to classify Drosophila into their correct age and genotype. The discriminant analysis was highly accurate, classifying Drosophila into their correct genotypic class at all age groups at 50–70% accuracy (20% chance baseline). Differences in cellular processes link to subtle alterations in neural network operation in young flies, all of which lead to the same pathogenic outcome. Our data are the first to quantify abnormal gain control and excitotoxicity in EOPD Drosophila mutants. We conclude that EOPD mutations may be linked to more sensitive neuronal signaling in prodromal animals that may cause the expression of PD symptomologies later in life. NEW & NOTEWORTHY Steady-state visually evoked potential response amplitudes to multivariate temporal contrast stimuli were recorded in early-onset PD Drosophila models. Our data indicate that abnormal gain control and a subsequent visual loss occur in these PD mutants, supporting a broader excitotoxicity hypothesis in genetic PD. Furthermore, linear discriminant analysis could accurately classify Drosophila into their correct genotype at different ages throughout their lifespan. Our results suggest increased neural signaling in prodromal PD patients.

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28

Dushay, Mitchell S., and Elizabeth D. Eldon. "Drosophila Immune Responses as Models for Human Immunity." American Journal of Human Genetics 62, no. 1 (January 1998): 10–14. http://dx.doi.org/10.1086/301694.

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29

Jackson, George R. "Guide to Understanding Drosophila Models of Neurodegenerative Diseases." PLoS Biology 6, no. 2 (February 26, 2008): e53. http://dx.doi.org/10.1371/journal.pbio.0060053.

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Gonzales, Erin, and Jerry Yin. "Drosophila Models of Huntington's Disease Exhibit Sleep Abnormalities." PLoS Currents 2 (September 29, 2010): RRN1185. http://dx.doi.org/10.1371/currents.rrn1185.

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31

Konsolaki, Mary, Ho-Juhn Song, Wesley Dobbs, and Dan Garza. "P2-109 Drosophila models of Alzheimer's-related pathways." Neurobiology of Aging 25 (July 2004): S255. http://dx.doi.org/10.1016/s0197-4580(04)80856-x.

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Chen, K. F., and D. C. Crowther. "Functional genomics in Drosophila models of human disease." Briefings in Functional Genomics 11, no. 5 (August 22, 2012): 405–15. http://dx.doi.org/10.1093/bfgp/els038.

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Iijima-Ando, Kanae, and Koichi Iijima. "Transgenic Drosophila models of Alzheimer’s disease and tauopathies." Brain Structure and Function 214, no. 2-3 (December 5, 2009): 245–62. http://dx.doi.org/10.1007/s00429-009-0234-4.

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Long, Zhe, Beisha Tang, and Hong Jiang. "Alleviating neurodegeneration in Drosophila models of PolyQ diseases." Cerebellum & Ataxias 1, no. 1 (2014): 9. http://dx.doi.org/10.1186/2053-8871-1-9.

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Moore, D. J. "Lessons from Drosophila Models of DJ-1 Deficiency." Science of Aging Knowledge Environment 2006, no. 2 (January 11, 2006): pe2. http://dx.doi.org/10.1126/sageke.2006.2.pe2.

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Rauzi, Matteo, Ana Hočevar Brezavšček, Primož Ziherl, and Maria Leptin. "Physical Models of Mesoderm Invagination in Drosophila Embryo." Biophysical Journal 105, no. 1 (July 2013): 3–10. http://dx.doi.org/10.1016/j.bpj.2013.05.039.

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Sanuki, Rikako. "i Drosophila i models of traumatic brain injury." Frontiers in Bioscience 25, no. 1 (2020): 168–78. http://dx.doi.org/10.2741/4801.

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38

Deng, Wu-Min. "Molecular genetics of cancer and tumorigenesis: Drosophila models." Journal of Genetics and Genomics 38, no. 10 (October 2011): 429–30. http://dx.doi.org/10.1016/j.jgg.2011.09.010.

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Kitani-Morii, Fukiko, and Yu-ichi Noto. "Recent Advances in Drosophila Models of Charcot-Marie-Tooth Disease." International Journal of Molecular Sciences 21, no. 19 (October 8, 2020): 7419. http://dx.doi.org/10.3390/ijms21197419.

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Charcot-Marie-Tooth disease (CMT) is one of the most common inherited peripheral neuropathies. CMT patients typically show slowly progressive muscle weakness and sensory loss in a distal dominant pattern in childhood. The diagnosis of CMT is based on clinical symptoms, electrophysiological examinations, and genetic testing. Advances in genetic testing technology have revealed the genetic heterogeneity of CMT; more than 100 genes containing the disease causative mutations have been identified. Because a single genetic alteration in CMT leads to progressive neurodegeneration, studies of CMT patients and their respective models revealed the genotype-phenotype relationships of targeted genes. Conventionally, rodents and cell lines have often been used to study the pathogenesis of CMT. Recently, Drosophila has also attracted attention as a CMT model. In this review, we outline the clinical characteristics of CMT, describe the advantages and disadvantages of using Drosophila in CMT studies, and introduce recent advances in CMT research that successfully applied the use of Drosophila, in areas such as molecules associated with mitochondria, endosomes/lysosomes, transfer RNA, axonal transport, and glucose metabolism.

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40

Li, Jing, Yu Wang, Cheng-Jie Zhu, Min Zhang, and Hao-Yuan Hu. "Offspring sex ratio shifts of the solitary parasitoid wasp, Trichopria drosophilae (Hymenoptera: Diapriidae), under local mate competition." Entomologica Fennica 29, no. 2 (June 17, 2018): 97–104. http://dx.doi.org/10.33338/ef.71221.

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Localmate competition (LMC) models predict a female-biased offspring sex ratio when a single foundress oviposits alone in a patch and an increasing proportion of sons with increasing foundress number. We tested whether the solitary pupal parasitoid, Trichopria drosophilae (Hymenoptera: Diapriidae), adjusted offspring sex ratio with foundress number when parasitizing Drosophila melanogaster pupae. Mean number of female offspring was higher than that of males, with a male proportion of 26 ± 16% when only one foundress oviposited. However, male proportion reached 58 ± 26%, 48 ± 22%, and 51 ± 19% in three-, five and seven-foundress cohorts. That the male proportion of offspring increased with foundress number is consistent with LMC models.

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41

Suzuki, Mari, Kazunori Sango та Yoshitaka Nagai. "Roles of α-Synuclein and Disease-Associated Factors in Drosophila Models of Parkinson’s Disease". International Journal of Molecular Sciences 23, № 3 (28 січня 2022): 1519. http://dx.doi.org/10.3390/ijms23031519.

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α-Synuclein (αSyn) plays a major role in the pathogenesis of Parkinson’s disease (PD), which is the second most common neurodegenerative disease after Alzheimer’s disease. The accumulation of αSyn is a pathological hallmark of PD, and mutations in the SNCA gene encoding αSyn cause familial forms of PD. Moreover, the ectopic expression of αSyn has been demonstrated to mimic several key aspects of PD in experimental model systems. Among the various model systems, Drosophila melanogaster has several advantages for modeling human neurodegenerative diseases. Drosophila has a well-defined nervous system, and numerous tools have been established for its genetic analyses. The rapid generation cycle and short lifespan of Drosophila renders them suitable for high-throughput analyses. PD model flies expressing αSyn have contributed to our understanding of the roles of various disease-associated factors, including genetic and nongenetic factors, in the pathogenesis of PD. In this review, we summarize the molecular pathomechanisms revealed to date using αSyn-expressing Drosophila models of PD, and discuss the possibilities of using these models to demonstrate the biological significance of disease-associated factors.

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42

Pruccoli, Letizia, Carlo Breda, Gabriella Teti, Mirella Falconi, Flaviano Giorgini, and Andrea Tarozzi. "Esculetin Provides Neuroprotection against Mutant Huntingtin-Induced Toxicity in Huntington’s Disease Models." Pharmaceuticals 14, no. 10 (October 13, 2021): 1044. http://dx.doi.org/10.3390/ph14101044.

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Huntington’s disease (HD) is a neurodegenerative disorder caused by an abnormal CAG trinucleotide repeat expansion within exon 1 of the huntingtin (HTT) gene. This mutation leads to the production of mutant HTT (mHTT) protein which triggers neuronal death through several mechanisms. Here, we investigated the neuroprotective effects of esculetin (ESC), a bioactive phenolic compound, in an inducible PC12 model and a transgenic Drosophila melanogaster model of HD, both of which express mHTT fragments. ESC partially inhibited the progression of mHTT aggregation and reduced neuronal death through its ability to counteract the oxidative stress and mitochondria impairment elicited by mHTT in the PC12 model. The ability of ESC to counteract neuronal death was also confirmed in the transgenic Drosophila model. Although ESC did not modify the lifespan of the transgenic Drosophila, it still seemed to have a positive impact on the HD phenotype of this model. Based on our findings, ESC may be further studied as a potential neuroprotective agent in a rodent transgenic model of HD.

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43

Innan, Hideki, and Wolfgang Stephan. "Distinguishing the Hitchhiking and Background Selection Models." Genetics 165, no. 4 (December 1, 2003): 2307–12. http://dx.doi.org/10.1093/genetics/165.4.2307.

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Abstract A simple method to distinguish hitchhiking and background selection is proposed. It is based on the observation that these models make different predictions about the average level of nucleotide diversity in regions of low recombination. The method is applied to data from Drosophila melanogaster and two highly selfing tomato species.

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44

Ogawa, Yukino, Kazuharu Arakawa, Kazunari Kaizu, Fumihiko Miyoshi, Yoichi Nakayama, and Masaru Tomita. "Comparative Study of Circadian Oscillatory Network Models of Drosophila." Artificial Life 14, no. 1 (January 2008): 29–48. http://dx.doi.org/10.1162/artl.2008.14.1.29.

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The circadian clock of Drosophila is a model pathway for research in biological clock mechanisms, both with traditional experimental approaches and with emerging systems biology approaches utilizing mathematical modeling and in silico computer simulation. Dynamic diurnal oscillations are achieved by the complex interaction of components as a system, and mathematical reconstruction has proven to be an invaluable means of understanding such systematic behavior. In this study, we implemented eight published models of the Drosophila circadian clock in Systems Biology Markup Language (SBML) for comparative systems biology studies using E-Cell Simulation Environment version 3, to examine the system-level requirements for the clock mechanism to be robust, by calculating the period and amplitude sensitivity coefficients with simulation experiments. While all models were generally robust as determined by the network topology of the oscillatory feedback loop structure, existing models place relatively strong emphasis on transcription regulation, although this is a limitation on robustness. We suggest that more comprehensive modeling including protein phosphorylation, polymerization, and nuclear transport with regard to amplitude sensitivity will be necessary for understanding the light entrainment and temperature compensation of circadian clocks.

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45

Mohan, Ryan D., Jerry L. Workman, and Susan M. Abmayr. "Drosophila models reveal novel insights into mechanisms underlying neurodegeneration." Fly 8, no. 3 (July 3, 2014): 148–52. http://dx.doi.org/10.4161/19336934.2014.969150.

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Bouleau, Sylvina, and Hervé Tricoire. "Drosophila Models of Alzheimer's Disease: Advances, Limits, and Perspectives." Journal of Alzheimer's Disease 45, no. 4 (April 13, 2015): 1015–38. http://dx.doi.org/10.3233/jad-142802.

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47

Tamura, Takuya, Masaki Sone, Takeshi Iwatsubo, Kazuhiko Tagawa, Erich E. Wanker, and Hitoshi Okazawa. "Ku70 Alleviates Neurodegeneration in Drosophila Models of Huntington's Disease." PLoS ONE 6, no. 11 (November 7, 2011): e27408. http://dx.doi.org/10.1371/journal.pone.0027408.

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48

Gonze, Didier, Jean-Christophe Leloup, and Albert Goldbeter. "Theoretical models for circadian rhythms in Neurospora and Drosophila." Comptes Rendus de l'Académie des Sciences - Series III - Sciences de la Vie 323, no. 1 (January 2000): 57–67. http://dx.doi.org/10.1016/s0764-4469(00)00111-6.

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Tan, Ying, Furong Yu, Andrea Pereira, Peter Morin, and Jianhua Zhou. "Suppression of Nrdp1 toxicity by Parkin in Drosophila models." Biochemical and Biophysical Research Communications 416, no. 1-2 (December 2011): 18–23. http://dx.doi.org/10.1016/j.bbrc.2011.10.104.

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50

McLeod, Catherine J., Louise V. O'Keefe, and Robert I. Richards. "The pathogenic agent in Drosophila models of ‘polyglutamine’ diseases." Human Molecular Genetics 14, no. 8 (March 7, 2005): 1041–48. http://dx.doi.org/10.1093/hmg/ddi096.

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