Journal
CELL
Volume 176, Issue 5, Pages 1083-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2019.01.018
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Funding
- SNSF [P2SKP3_148494, P300PA_160996, P2EZP3_ 172142]
- EMBO [ALTF 33-2013]
- NIH [HD085866, GM46498, K01 DK098285, 1U54CA217377, AG011085]
- Wellcome Trust Sir Henry Postdoctoral Fellowship [110275/Z/15/Z]
- Francis Crick Institute from Cancer Research UK [FC001203]
- UK Medical Research Council [FC001203]
- Wellcome Trust [FC001203]
- NSF graduate research fellowship [DGE 1342536]
- William Bowes Fellows program
- Vilcek Foundation
- HHMI HCIA Summer Institute
- Swiss National Science Foundation (SNF) [P300PA_160996, P2EZP3_172142, P2SKP3_148494] Funding Source: Swiss National Science Foundation (SNF)
- Wellcome Trust [110275/Z/15/Z] Funding Source: Wellcome Trust
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Cell size varies greatly between cell types, yet within a specific cell type and growth condition, cell size is narrowly distributed. Why maintenance of a cell-type specific cell size is important remains poorly understood. Here we show that growing budding yeast and primary mammalian cells beyond a certain size impairs gene induction, cell-cycle progression, and cell signaling. These defects are due to the inability of large cells to scale nucleic acid and protein biosynthesis in accordance with cell volume increase, which effectively leads to cytoplasm dilution. We further show that loss of scaling beyond a certain critical size is due to DNA becoming limiting. Based on the observation that senescent cells are large and exhibit many of the phenotypes of large cells, we propose that the range of DNA: cytoplasm ratio that supports optimal cell function is limited and that ratios outside these bounds contribute to aging.
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