Transposable element activation promotes neurodegeneration in a Drosophila model of Huntington's disease
Assunta Maria Casale, Francesco Liguori, Federico Ansaloni, Ugo Cappucci, Sara Finaurini, Giovanni Spirito, Francesca Persichetti, Remo Sanges, Stefano Gustincich, Lucia Piacentini
Abstract
HD model. By inhibiting TE mobilization with Reverse Transcriptase inhibitors, polyQ-dependent eye neurodegeneration and genome instability in larval brains are rescued and fly lifespan is increased. These results suggest that TE activation may be involved in polyQ-induced neurotoxicity and a potential pharmacological target.
Topics & Concepts
NeurodegenerationTransposable elementDrosophila (subgenus)Huntington's diseaseDNA Transposable ElementsBiologyNeuroscienceGeneticsDiseaseGenomeMedicineGeneInternal medicineChromosomal and Genetic VariationsGenetic Neurodegenerative DiseasesCRISPR and Genetic Engineering