Centromeric signaling proteins boost G1 cyclin degradation and modulate cell size in budding yeast

PLoS Biol. 2018 Aug 6;16(8):e2005388. doi: 10.1371/journal.pbio.2005388. eCollection 2018 Aug.


Cell size scales with ploidy in a great range of eukaryotes, but the underlying mechanisms remain unknown. Using various orthogonal single-cell approaches, we show that cell size increases linearly with centromere (CEN) copy number in budding yeast. This effect is due to a G1 delay mediated by increased degradation of Cln3, the most upstream G1 cyclin acting at Start, and specific centromeric signaling proteins, namely Mad3 and Bub3. Mad3 binds both Cln3 and Cdc4, the adaptor component of the Skp1/Cul1/F-box (SCF) complex that targets Cln3 for degradation, these interactions being essential for the CEN-dosage dependent effects on cell size. Our results reveal a pathway that modulates cell size as a function of CEN number, and we speculate that, in cooperation with other CEN-independent mechanisms, it could assist the cell to attain efficient mass/ploidy ratios.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle Proteins / metabolism
  • Cell Division
  • Cell Enlargement
  • Cell Growth Processes / physiology*
  • Centromere / metabolism
  • Centromere / physiology*
  • Cyclin G1 / metabolism*
  • Cyclins / metabolism
  • G1 Phase / physiology
  • Gene Expression Regulation, Fungal
  • Membrane Glycoproteins / metabolism
  • Membrane Glycoproteins / physiology
  • Nuclear Proteins / metabolism
  • Proteolysis
  • Saccharomyces cerevisiae / metabolism
  • Saccharomyces cerevisiae Proteins / metabolism
  • Saccharomycetales / metabolism
  • Signal Transduction


  • BUB3 protein, S cerevisiae
  • Cell Cycle Proteins
  • Cyclin G1
  • Cyclins
  • MAD3 protein, S cerevisiae
  • Membrane Glycoproteins
  • Nuclear Proteins
  • Saccharomyces cerevisiae Proteins

Grant support

Ministry of Economy and Competitiveness of Spain (grant number BFU2016-80234-R to MA and BFU 2013-44189-P to JC). JMM-L and DFM acknowledge fellowhips of the FI program of Generalitat de Catalunya. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.