摘要：SummaryBabies are born young, largely independent of the age of their mothers. Mother-daughter age asymmetry in yeast is achieved, in part, by inheritance of higher-functioning mitochondria by buds and retention of some high-functioning mitochondria in mother cells. The mitochondrial F box protein, Mfb1p, tethers mitochondria at both poles in a cell cycle-regulated manner: it localizes to and anchors mitochondria at the mother cell tip throughout the cell cycle and at the bud tip before cytokinesis. Here, we report that cell polarity and polarized localization of Mfb1p decline with age inSaccharomyces cerevisiae. Moreover, deletion of genes (BUD1,BUD2,andBUD5) that mediate symmetry breaking during establishment of cell polarity and asymmetric yeast cell division cause depolarized Mfb1p localization and defects in mitochondrial distribution and quality control. Our results support a role for the polarity machinery in lifespan through modulating Mfb1 function in asymmetric inheritance of mitochondria during yeast cell division.Graphical abstractDisplay OmittedHighlights•Budding polarity declines with age•Polarization of a mitochondrial tether, Mfb1p, within mother cells declines with age•Defects in budding polarity disrupt Mfb1p polarization and mitochondrial distribution•Polarity defects affect Mfb1p-mediated mitochondrial quality and lifespan controlBiological sciences; Genetics; Molecular biology; Cell biology
