Fig. 3

Schematic representation of asymmetric inheritance of damaged/aggregated proteins and protective molecules during yeast and mammalian cell division. In yeast, a misfolded and oxidatively damaged proteins form aggregates that preferentially accumulate in mother cells (long lived) not entering in the bud. At the same time, there is an increased catalase concentration in the bud contributing to the reduced levels of H₂O₂ found in the daughter cell. This asymmetrical distribution is dependent on the actin cytoskeleton, molecular chaperones (e.g., Hsp40), and the NAD⁺-dependent histone deacetylase Sir2p. Similarly, in mammalian cells, b aggresomes (damaged proteins) are asymmetrically distributed to one of the daughter cells and concentrate close to the centrosome. This transport relies on dynein/dynactin complexes and on the microtubule cytoskeleton. In both types of cells, the asymmetrical distribution of damaged materials and protective molecules seems to be an important event for cell aging. A similar mechanism may possibly be used by adult mammalian stem cells in order to protect their self-renewing progeny of damaged molecules. For more details, please see the text