A transgenic Drosophila melanogaster model to study human T-lymphotropic virus oncoprotein Tax-1-driven transformation in vivo
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Authors
Shirinian, Margret
Kambris, Zakaria
Hamadeh, Lama N.
Grabbe, Caroline
Journo, Chloé
Mahieux, Renaud
Bazarbachi, Ali Abdul Hamid
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Publisher
American Society for Microbiology
Abstract
Human T-cell lymphotropic virus type 1 (HTLV-1)-induced adult T-cell leukemia/lymphoma is an aggressive malignancy. HTLV-2 is genetically related to HTLV-1 but does not cause any malignant disease. HTLV-1 Tax transactivator (Tax-1) contributes to leukemogenesis via NF-κB. We describe transgenic Drosophila models expressing Tax in the compound eye and plasmatocytes. We demonstrate that Tax-1 but not Tax-2 induces ommatidial perturbation and increased plasmatocyte proliferation and that the eye phenotype is dependent on Kenny (IKKγ/NEMO), thus validating this new in vivo model. © 2015, American Society for Microbiology.
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Keywords
Animals, Cell transformation, viral, Disease models, animal, Drosophila melanogaster, Eye, Gene products, tax, Htlv-i infections, Human t-lymphotropic virus 1, Human t-lymphotropic virus 2, Humans, I kappa b kinase gamma, Oncoprotein, Protein tax 1, Protein tax 2, Transactivator protein, Unclassified drug, Tax protein, Tax protein, human t-lymphotrophic virus 1, Tax protein, human t-lymphotrophic virus 2, Animal cell, Animal experiment, Animal model, Animal tissue, Article, Cell proliferation, Cell transformation, Controlled study, Disease model, Disease severity, Eye development, Eye disease, Gal4 gene, Gene, Gene dosage, Gene expression regulation, Gene function, Gene identification, Gene interaction, Gene overexpression, Gmr gene, In vivo study, Lymphocyte transformation, Molecular cloning, Nonhuman, Oncogene, Phenotype, Plasma cell, Priority journal, Promoter region, Protein function, Protein protein interaction, Rna interference, Rough eye disease, Scanning electron microscopy, Tax 1 gene, Transcription regulation, Transgenic drosophila, Animal, Genetics, Human, Human t cell leukemia virus infection, Metabolism, Pathology, Physiology, Virology, Virus cell transformation