In order to delay aging, the process of aging must first be understood; that the aging of cells is what drives the aging of an organism. Recent aging research studies have shown that cellular aging and asymmetric cell division are intimately linked. Yeast has been the ideal model for replicative aging because it undergoes asymmetric cell division. In budding yeast, asymmetric cell division yields a mother cell and a daughter cell that are easily distinguishable under a microscope, giving scientists the opportunity to compare the two cells and further understand aging at a molecular level. Tracking the fate of the mother lineage has led to the discovery that individual mother cells have a fixed replicative lifespan, defined by the number of daughters a mother cell produces before deterioration. Although mother cells age with each division, their daughters retain the same full lifespan independent of the age of the mother. Thus, the asymmetry in cell division leads to asymmetry of aging.

In this study, Jing Yang et al. took a proteome-centric approach to explore cell division asymmetry and its connection to lifespan asymmetry in budding yeast. They found that mother-enriched proteins tend to accumulate in mother cells over time using an active sorting mechanism, a process that has been linked to aging in these cells. Mother cells age because they retain damaged, or lifespan-limiting, proteins, so that their daughters start out with a younger, ‘reset’ physiology. These observations provide a consistent picture of how asymmetric dividing of the proteome influences lifespan asymmetry, and serve as a starting point for generating new hypotheses on the mechanism of asymmetry and aging.

Studying why and how these aging-related traits happen in yeast may provide interesting avenues of future research in higher organisms. Observations from this study support the general notion that mother cells retain aging factors to themselves, enabling their daughters to rejuvenate. However, a global view of the identities of asymmetrically partitioned aging factors and the mechanism through which they influence lifespan is still lacking. Clearly, there is still more to be gained from yeast for understanding human aging, what causes it, and how it can be delayed.