Mitochondrial quality control during inheritance is associated with lifespan and mother-daughter age asymmetry in budding yeast.

Ageing is an accumulation of damaged biomolecules that results in reduced or aberrant function of cells and, ultimately, an organism. During gamete formation, or in asexually propagating species, age must be reversed to make the new organism young. How are old or damaged components recognized and prevented from being passed on to the new organism? McFaline-Figueroa et al. find that, in the rejuvenating asymmetric cell divisions of Saccharomyces cerevisiae, dysfunctional mitochondria are retained in the mother cell to promote fitness and long life of the bud cell.

Important targets of age-accumulated damage are mitochondria, which, when compromised, can generate reactive oxygen species that negatively affect a variety of biomolecules. An essential question is, how are mitochondria selected for or against when organisms undergo rejuvenation? Normal proliferative growth of S. cerevisiae comprises a rejuvenation mechanism, in that ageing-associated components - such as rDNA circles and damaged proteins - are retained in the mother cell, generating a comparatively 'young' bud cell. McFaline-Figueroa et al. test the role of asymmetric mitochondrial segregation in controlling the lifespan of S. cerevisiae, finding that a failure to retain damaged mitochondria in the mother cell reduces the fitness and lifespan of the bud cell. Here, mother-bud mitochondrial asymmetry was detected by differences in superoxide levels and redox potential (and, previously, by membrane potential). An interesting open question is how such metabolic differences are recognized by the mitochondria segregation machinery in the cell. The findings have important implications for sexual reproduction and the almost universal feature of paternal mitochondria elimination from zygotes - are paternal mitochondria also 'old' or damaged and are they recognized by the same features? And there is the question of whether similar mitochondria quality controls function in asymmetric stem cell divisions in various developmental contexts, either to increase the fitness of progeny by making them 'young', or, conversely, to maintain the 'youth' of the stem cell itself.