Abstract
An asymmetry in cytosolic pH between mother and daughter cells was reported to underlie cellular aging in the budding yeast Saccharomyces cerevisiae; however, the underlying mechanism remains unknown. Preferential accumulation of Pma1p, which pumps cytoplasmic protons out of cells, at the plasma membrane of mother cells, but not of their newly-formed daughter cells, is believed to be responsible for the pH increase in mother cells by reducing the level of cytoplasmic protons. This, in turn, decreases the acidity of vacuoles, which is well correlated with aging of yeast cells. In this study, to identify genes that regulate the preferential accumulation of Pma1p in mother cells, we performed a genome-wide screen using a collection of single gene deletion yeast strains. A subset of genes involved in the endocytic pathway, such as VPS8, VPS9, and VPS21, was important for Pma1p accumulation. Unexpectedly, however, there was little correlation between deletion of each of these genes and the replicative lifespan of yeast, suggesting that Pma1p accumulation in mother cells is not the key determinant that underlies aging of mother cells.
Highlights
Cellular aging is a fundamental process that contributes to the complicated aging process at the organismal level [1]
According to studies performed by Gottschling and colleagues [7,8,11], Pma1p preferentially accumulates at the plasma membrane of mother cells during cell divisions, and the resulting decreased concentration of cytoplasmic protons leads to a scarcity of vacuolar protons, which eventually increases vacuolar pH
The plasma membrane protein Pma1p asymmetrically accumulates in the mother cell, instead of being evenly distributed between mother and daughter cells, in the budding yeast Saccharomyces cerevisiae [7]
Summary
Cellular aging is a fundamental process that contributes to the complicated aging process at the organismal level [1]. This increase in vacuolar pH decreases the mitochondrial membrane potential in mother cells by unknown mechanisms [8] These dual defects in vacuoles and mitochondria may contribute to aging of mother cells. Daughter cells are generated largely free of aging factors after every division This phenomenon is termed rejuvenation of daughter cells and is partly achieved by retention of damaged mitochondria [9] and the plasma membrane proton pump Pma1p [7], preferentially in mother cells. According to studies performed by Gottschling and colleagues [7,8,11], Pma1p preferentially accumulates at the plasma membrane of mother cells during cell divisions, and the resulting decreased concentration of cytoplasmic protons leads to a scarcity of vacuolar protons, which eventually increases vacuolar pH. In this study, using a collection of single gene deletion yeast strains, we performed a genome-wide screen for genes that regulate the preferential accumulation of Pma1p at the plasma membrane of mother cells and identified a series of genes involved in the endocytic pathway as candidate genes that may regulate aging of yeast cells
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