Abstract
Aging Following the fate of individual yeast cells has revealed aging to be more of a programmable decision process rather than a simple accumulation of deleterious events. Li et al. combined single-cell studies and mathematical modeling to show that yeast cells showed two different forms of aging: one with less ribosomal DNA silencing, in which nucleoli were degraded, and another with less heme accumulation and hemedependent transcription, in which mitochondria were more affected. Overexpression of the lysine deacetylase Sir2, which contributes to ribosomal DNA silencing, led to a third cell-aging fate in which the average life span was extended. If other cells age in similar ways, then this study may provide new ways to consider dynamics of aging and strategies to extend the health span. Science this issue p. [325][1] [1]: /lookup/doi/10.1126/science.aax9552
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