HETEROLOGOUS EXPRESSION OF TAU PROTEIN IN FISSION YEAST AS A DISEASE MODEL

Abstract

Alzheimer's disease (AD) is a common neurodegenerative disease associated with aging. Two prominent hallmarks of the disease are the accumulations of the beta-amyloid peptide (A beta) plaques and the tangles of the microtubule-associated protein tau. Mutations in the human mapt gene show that molecular tau pathology can also cause neurodegeneration without A beta plaques formation, and that tau protein is involved in most neurodegenerative disease pathologies. Thus far, majority of the Alzheimer's disease studies has focused on understanding the A beta-plaque formation and developing therapies to prevent its accumulation. In recent years, however, other proteins that are involved in the Alzheimer's disease pathologies, such as tau, have gained importance. Endogenous or heterologous proteins that are implicated in neurodegenerative diseases have widely been investigated by using yeast models. In this study, we aimed to construct a favorable model by transferring the human inapt gene to Schizosaccharomyces pombe to study the basic mechanisms related to tau protein in cell.