The degradation of intracellular proteins is a fundamental biological process necessary for maintaining cellular homeostasis, controlling the cell cycle, regulating signal transduction, and preventing the accumulation of toxic protein aggregates. Disorders of the proteolytic systems are implicated in the pathogenesis of numerous human diseases, including neurodegenerative diseases, lysosomal storage disorders, metabolic disorders, and certain types of cancer. The development of rudimentary and cost-effective models of these diseases for the purpose of evaluating novel pharmaceutical agents and elucidating the molecular mechanisms underlying disease pathogenesis constitutes a pivotal medical and biological undertaking. The proteolytic apparatus of the yeast species Saccharomyces cerevisiae has become a biochemical model organism of significant importance. This is due to its well-studied nature, low cost, ease of genetic manipulation, and evolutionary conservatism. The mechanisms of proteolytic system dysfunction can be studied in this organism. Furthermore, therapeutic approaches aimed at correcting these dysfunctional mechanisms can be sought.
Sosnovtseva et al. (Mon,) studied this question.