Drosophila melanogaster Model in Neurodegenerative Disease Research

Yıl 2020, Cilt: 46 Sayı: 2, 237 - 245, 01.08.2020

Cem Hazır Gamze Bora , Hayat Erdem Yurter

https://doi.org/10.32708/uutfd.732671

Cited By: 1

Öz

Modelling human diseases in Drosophila melanogaster have been accelerated advances in many areas including investigations on pathophysiology, identification of new genes and genetic modifiers, explanations of clinic variability, development of new diagnosis and treatment approaches and drug investigations. In this review, advantages of D. melanogaster as a model organism and its use in neurodegenerative diseases are discussed.

Modelling human diseases in Drosophila melanogaster have been accelerated advances in many areas including investigations on pathophysiology, identification of new genes and genetic modifiers, explanations of clinic variability, development of new diagnosis and treatment approaches and drug investigations. In this review, advantages of D. melanogaster as a model organism and its use in neurodegenerative diseases are discussed.

Anahtar Kelimeler

Drosophila melanogaster, model organism, neurodegenerative disease, genetics

Nörodejeneratif Hastalık Araştırmalarında Drosophila melanogaster Modeli

Öz

İnsan hastalıklarının Drosophila melanogaster’de modellenmesi sayesinde, patofizyolojilerin araştırılması, yeni genlerin ve genetik düzenleyicilerin tanımlanması, klinik çeşitlilik nedenlerinin açıklanabilmesi, yeni tanı ve tedavi yaklaşımlarının geliştirilmesi, ilaç araştırma çalışmalarının yapılabilmesi gibi birçok alandaki gelişmeler hız kazanmıştır. Bu derlemede D. melaonogaster’in model organizma olarak avantajları ve nörodejeneratif hastalıklarla ilişkili araştırmalarda kullanılmasına ilişkin bilgiler verilmektedir.

Anahtar Kelimeler

Drosophila melanogaster, model organizma, nörodejeneratif hastalık, genetik

Kaynakça

• 1. Jenning BH. Drosophila – a versatile model in biology and medicine. Materials Today. 2011;14:190-195.
• 2. The Nobel Price in Physiology or Medicine (1933). https://www.nobelprize.org/prizes/medicine/1933/summary/
• 3. Tolwinski NS. Introduction: Drosophila- a model system for developmental biology. J Dev Biol. 2017;5:9.
• 4. Allocca M, Zola S, Bellosta P. The fruit fly, Drosophila melanogaster: the making of a model (Part I). In: Perveen FK, (eds). Drosophila melanogaster: Model for Recent Advances in Genetics and Therapeutics. Rijeka, Croatia: InTech;2018:113-130.
• 5. Ankeny RA, Leonelli S. What’s so special about model organisms. Studies in History and Philosophy of Science. 2011;42:314-323.
• 6. Hedges SB. The origin and evolution of model organisms. Nature. 2002;3:838-849.
• 7. Bachli G. TaxoDros: The database on taxonomy of Drosophilidae, (taxodros.uzh.cs). (1999-2006).
• 8. Gonzalez C. Drosophila melanogaster: a model and tool to investigate malignancy and identify new therapeutics. Nature Rev. 2013;13:172-183.
• 9. McGurk L, Berson A, Bonini NM. Drosophila as in vivo model for human neurodegenerative disease. Genetics. 2015;201:377-402.
• 10. Sang TK, Jackson RG. Drosophila models of neurodegenerative disease. The Journal of the American Society for Experimental NeuroTherapeutics. 2005;2:438-446.
• 11. Pandey UB, Nichols CD. Human disease models in Drosophila melanogaster and the role of the fly in therapeutic drug discovery. Pharmacol Rev. 2011;63:412-431.
• 12. Baenas N, Wagner AE. Drosophila melanogaster as an alternative model organism in nutrigenomics. Genes Nutr. 2019;14:1-11.
• 13. Moreno MA, Farr CL, Kaguni LS, Garesse R. Drosophila melanogaster as a model system to study mitochondrial biology. Methods Mol Biol. 2007;372:33-49.
• 14. Flatt T. Life history evolution and the genetics of fitness components in Drosophila melanogaster. Genetics. 2020:214:3-48.
• 15. He Y, Jasper H. Studying aging in Drosophila. Methods. 2014;68:129–133.
• 16. Ryvkin J, Bentzur A, Krispil SZ, Ophir GS. Mechanisms underlying the risk to develop drug addiction, insights from studies in Drosophila melanogaster. Front Physiol. 2018;9:1-12.
• 17. Yamaguchi M, (eds). Drosophila models for human diseases. 1st edition. Singapore: Springer; 2018.
• 18. Potter CJ, Turenchalk GS, Xu T. Drosophila in cancer research an expanding role. Trends in Genetics. 2000;16:33-39.
• 19. Villegas SN. One hundred years of Drosophila cancer research: no longer in solidute. Disease Models and Mechanisms. 2019;12:1-5.
• 20. Bodmer R. The gene tinman is required for specification of the heart and visceral muscles in Drosophila. Development. 1993;118:719-729.
• 21. Allocca M, Zola S, Bellosta P. The fruit fly, Drosophila melanogaster: modeling of human diseases (Part II). In: Perveen FK, (eds). Drosophila melanogaster: Model for Recent Advances in Genetics and Therapeutics. Rijeka, Croatia: In Tech; 2018:131-156.
• 22. Bergman P, Esfahani SS, Engstrom Y. Drosophila as a model for human diseases—focus on innate immunity in barrier epithelia, Curr Top Dev Biol. 2017;121:30-66.
• 23. Gitler AD, Dhillon P, Shorter J. Neurodegenerative disease: models, mechanisms and a new hope. Dis Models Mech. 2017;10:499-502.
• 24. Peng C, Trojanowski JQ, Lee VM. Protein transmission in neurodegenerative disease. Nature. 2020;16:199-212.
• 25. Aquilina B, Cauchci RJ. Modelling motor neuron disease in fruit flies: Lessons from spinal muscular atrophy. J Neurosci Methods. 2018;310:3-11.
• 26. Ugur B, Chen K, Bellen HJ. Drosophila tools and assays for the study of human diseases, disease models and mechanisms. Dis Model Mech. 2016;9:235-244.
• 27. Cartegni L, Krainer AR. Disruption of an SF2/ASF-dependent exonic splicing enhancer in SMN2 causes spinal muscular atrophy in the absence of SMN1. Nature. 2002;30:377-384.
• 28. Lefebvre S, Burglen L, Reboullet S, ve ark. Identification and characterization of a spinal muscular atrophy-determining gene. Cell. 1995;80:155–165.
• 29. Melki J, Lefebvre S, Burglen L, ve ark. De novo and inherited deletions of the 5q13 region in spinal muscular atrophies. Science. 1994;264:1474-1477.
• 30. Groen EJN, Talbot K, Gillingwater TH. Advances in theraphy for spinal muscular atrophy: promises and challenges. Nature Rev Neurol. 2018;14:214-224.
• 31. Kreipke RE, Kwon YV, Shcherbata HR, Baker HR. Drosophila melanogaster as a model of muscle degeneration disorders. Current Topics in Developmental Biology. 2017;121:83-109.
• 32. Chang HC, Dimlich DN, Yokokura T, ve ark. Modelling spinal muscular atrophy in Drosophila. PLoS ONE. 2008;3:1-18.
• 33. Lloyd TE, Taylor JP. Flightless flies: Drosophila models of neuromuscular disease. Ann N Y Acad Sci. 2010;1184:1-25.
• 34. Sen A, Yokokura T, Kankel MW, ve ark. Modeling spinal muscular atrophy in Drosophila links Smn to FGF signaling. J Cell Biol. 2011;192:481-495.
• 35. Martin S, Khleifat AA, Chalabi AA. What causes amyotrophic lateral sclerosis. F1000Res. 2017;6:1-10. 36. Blacher E, Bashiardes S, Shapiro H, ve ark. Potential roles of gut microbiome and metabolites in modulating ALS in mice. Nature. 2019;572:474-480.
• 37. Tortarolo M, Coco DL, Veglianese P, ve ark. Amyotrophic lateral sclerosis a multisystem pathology: Insights into the role of TNFα. Mediators of Inflammation. 2017;2017:1-16.
• 38. Casci I, Pandey UB. A fruit fly endeavor: Modeling ALS in the fruitfly. Brain Res. 2015;1607:1-28.
• 39. Watson MR, Lagow RD, Xu K, Zhang B, Bonini NM. A drosophila model for amyotrophic lateral sclerosis reveals motor neuron damage by human SOD1. J Biol Chem. 2008;283:24972–24981.
• 40. Bahadorani S, Mukai ST, Rabie J, ve ark. Expression of zinc-deficient human superoxide dismutase in Drosophila neurons produces a locomotor defect linked to mitochondrial dysfunction. Neurobiol Aging. 2013;34:2322–2330.
• 41. Chai A, Withers J, Koh YH, ve ark. hVAPB, the causative gene of a heterogeneous group of motor neuron diseases in humans, is functionally interchangeable with its Drosophila homologue DVAP-33A at the neuromuscular junction. Hum Mol Genet. 2008;17:266-280.
• 42. Ratnaparkhi A, Lawless GM, Schweizer FE, Golshani P, Jackson GR. Drosophila model of ALS: Human ALS-associated mutation in VAP33A suggests a dominant negative mechanism. PLoS ONE. 2008;3:1-13.
• 43. Diaper DC, Adachi Y, Lazarou L, ve ark. Drosophila TDP-43 dysfunction in glia and muscle cells cause cytological and behavioural phenotypes that characterize ALS and FTLD. Hum Mol Genet. 2013;22:883–3893.
• 44. Elden AC, Kim HJ, Hart MP, ve ark. Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS. Nature. 2010;466:1070-1077.
• 45. Radhakrishnan DM, Goyal V. Parkinson's disease: A review. Neurol India. 2018;66:26‐35.
• 46. Yamaguchi M, (eds). Drosophila models for human diseases. 1st edition. Singapore: Springer; 2018.
• 47. Baroli B, Loi E, Solari P, ve ark. Evaluation of oxidative stress mechanisms and the effects of phytotherapic extracts on Parkinson’s disease Drosophila PINK1B9 model. FASEB J. 2019;33:11028-11034
• 48. DeMaagd G, Philip A. Parkinson’s disease and its management. P & T. 2015;40:504-532
• 49. Wang D, Tang B, Zhao G, ve ark. Dispensable role of Drosophila ortholog of LRRK2 kinase activity in survival of dopaminergic neurons. Mol Neurodegener. 2008;3:1-7
• 50. Poole AC, Thomas RE, Andrews LA, ve ark. The PINK1/Parkin pathway regulates mitochondrial morphology. Proc Natl Acad Sci U S A. 2008;105:1638–1643. 51. Xiong Y, Yu J. (2018) Modeling Parkinson’s disease in Drosophila: What have we learned from dominant traits?. Front Neurol. 2018;9:1-15
• 52. Pesah Y, Pham T, Burgess H, ve ark. Drosophila parkin mutants have decreased mass and cell size and increased sensitivity to oxygen radical stress. Development. 2004;131:2183–2194
• 53. Greene J., Whitworth A., Kuo I, ve ark. Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants. Proc Natl Acad Sci U S A. 2003;100:4078–4083
• 54. Deng H, Dodson M, Huang H, Guo M. The Parkinson's disease genes Pink1 and Parkin promote mitochondrial fission and/or inhibit fusion in Drosophila. Proc Natl Acad Sci U S A. 2008;105: 14503– 14508.
• 55. Auluck PK, Chan HY, Trojanowski JQ, Bonini NM, Lee VM. Chaperone supression of alpha synuclein toxicity in a Drosophila model for Parkinson’s disease. Science. 2002;295:865-868
• 56. Auluck PK., Bonini NM, Meulener MC. Mechanism of supression of alpha synuclein neuro toxicity by geldanamycin in Drosophila. J Biol Chem. 2005;280:2873-2878
• 57. Soriano VM, Paricio N. Drosophila models of Parkinson’s disease: Discovering relevant pathways and novel therapeutic strategies. Parkinsons Dis. 2011; 2011:1-14
• 58. Khanahmadi M, Farhud DD, Malmir M. Genetic of Alzheimer’s disease: A narrative review article. Iran J of Public Health. 2015;44:892-901
• 59. Yamaguchi M, (eds). Drosophila models for human diseases. 1st edition. Singapore: Springer; 2018.
• 60. Ulep MG, Saraon SK, Mclea S. Alzheimer disease. The Journal for Nurse Practitioners. 2018;14:129-135
• 61. Tue NT, Dat TQ, Ly LL, Anh VD, Yoshida H. Insights from Drosophila melanogaster model of Alzheimer's disease. Front Biosci. 2020;25:134-146
• 62. Tan FHP, Azzam G. Drosophila melanogaster: Deciphering Alzheimer’s disease. Malays J Med Sci. 2017;24:6-20
• 63. Buhl E, Higham JP, Hodge JJL. Alzheimer's disease-associated tau alters Drosophila circadian activity, sleep and clock neuron electrophysiology. Neurobiol Dis. 2019;130:1-9
• 64. Prüßing K, Voigt A, Schulz JB. Drosophila melanogaster as a model organism for Alzheimer’s disease. Mol Neurodegener. 2013;8:2-11
• 65. Iijima K, Liu HP, Chiang AS, ve ark. Dissecting the pathological effects of human Aß40 and Aß42 in Drosophila: A potential model for Alzheimer’s disease. Proc Natl Acad Sci U S A. 2004; 101:6623-6628
• 66. Greeve I, Kretzschmar D, Tschäpe JA, ve ark. Age-dependent neurodegeneration and Alzheimer-amyloid plaque formation in transgenic Drosophila. J Neurosci. 2004;24:3899–3906.