Accelerated aging and failure to segregate damaged proteins in Sir2 mutants can be suppressed by overproducing the protein aggregation-remodeling factor Hsp104p

A study to show that carbonylated proteins are associated with Hsp104p-cointaining protein aggregates and that these aggregates are retained in progenitor cell during cytokinesis by a Sir2p-dependent process is conducted. Results show that deletion of HSP104 resulted in breakdown of damage asymmetry, and overproduction of Hsp104p partially restored damage retention.