Accumulation of damaged proteins is a hallmark of ageing, occurring in organisms ranging from bacteria and yeast to mammalian cells. During cell division in Saccharomyces cerevisiae, damaged proteins are retained within the mother cell, resulting in an ageing mother while a new daughter cell exhibits full replicative potential. The cell-specific features determining the ageing remain elusive. It has been suggested that the replicative ageing is dependent on the ability of the cell to repair and retain pre-existing damage. To deepen the understanding of how these factors influence the life of individual cells, we developed and experimentally validated a dynamic model of damage accumulation accounting for replicative ageing on the single cell level. The model includes five essential properties: cell growth, damage formation, damage repair, cell division and cell death, represented in a theoretical framework describing the conditions allowing for replicative ageing, starvation, immortality or clonal senescence. We introduce the resilience to damage, which can be interpreted as the difference in volume between an old and a young cell. We show that the capacity to retain damage deteriorates with high age, that asymmetric division allows for retention of damage, and that there is a trade-off between retention and the resilience property. Finally, we derive the maximal degree of asymmetry as a function of resilience, proposing that asymmetric cell division is beneficial with respect to replicative ageing as it increases the lifespan of a given organism. The proposed model contributes to a deeper understanding of the ageing process in eukaryotic organisms. Cell division, growth and death are fundamental features of any living organism. During its life cycle, a cell produces a set of functional components such as proteins or other metabolites, which will ultimately allow the cell to divide, giving rise to a newly born daughter cell. However, due to inherent imperfections in the cellular machinery over time, cells are slowly deteriorating causing essential intracellular functions to perish. At the very end of a cell's lifespan, age-associated damage builds up consistently impairing the ability of the cell to divide and survive, which eventually culminates in cell death. In environments with a sufficient amount of food, damage will be formed as a consequence of cell growth. This causes the partitioning of damage between the progenitor and progeny during cell division to be an important function. An asymmetric distribution of cell mass after division constitutes a vital part of ageing in the yeast Saccharomyces cerevisiae (S.cerevisiae). The number of divisions before cell death is a measure of the age of a single yeast cell, which has been studied substantially by means of experiments 1,2 , and it is called the replicative life span (RLS). The asymmetric division of the budding yeast results in a large ageing mother cell with a finite RLS and a new small daughter cell with full replicative potential 3. Replicative ageing in...