Growth-dependent signals drive an increase in early G1 cyclin concentration to link cell cycle entry with cell growth

  1. Robert A Sommer
  2. Jerry T DeWitt
  3. Raymond Tan
  4. Douglas R Kellogg  Is a corresponding author
  1. University of California, Santa Cruz, United States

Abstract

Entry into the cell cycle occurs only when sufficient growth has occurred. In budding yeast, the cyclin Cln3 is thought to initiate cell cycle entry by inactivating a transcriptional repressor called Whi5. Growth-dependent changes in the concentrations of Cln3 or Whi5 have been proposed to link cell cycle entry to cell growth. However, there are conflicting reports regarding the behavior and roles of Cln3 and Whi5. Here, we found no evidence that changes in the concentration of Whi5 play a major role in controlling cell cycle entry. Rather, the data suggest that cell growth triggers cell cycle entry by driving an increase in the concentration of Cln3. We further found that accumulation of Cln3 is dependent upon homologs of mammalian SGK kinases that control cell growth and size. Together, the data are consistent with models in which Cln3 is a crucial link between cell growth and the cell cycle.

Data availability

Figures present data from biological replicates that are representative of multiple biological replicates. Coulter counter data show the average of multiple biological replicates.

Article and author information

Author details

  1. Robert A Sommer

    Molecular, Cell and Developmental Biology, University of California, Santa Cruz, Santa Cruz, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Jerry T DeWitt

    Molecular, Cell and Developmental Biology, University of California, Santa Cruz, Santa Cruz, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-9077-643X
  3. Raymond Tan

    Molecular, Cell and Developmental Biology, University of California, Santa Cruz, Santa Cruz, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. Douglas R Kellogg

    Molecular, Cell and Developmental Biology, University of California, Santa Cruz, Santa Cruz, United States
    For correspondence
    dkellogg@ucsc.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-5050-2194

Funding

National Institutes of Health (GM053959)

  • Douglas R Kellogg

National Institutes of Health (GM131826)

  • Douglas R Kellogg

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Naama Barkai, Weizmann Institute of Science, Israel

Publication history

  1. Preprint posted: October 1, 2020 (view preprint)
  2. Received: October 27, 2020
  3. Accepted: October 29, 2021
  4. Accepted Manuscript published: October 29, 2021 (version 1)
  5. Accepted Manuscript updated: November 1, 2021 (version 2)
  6. Version of Record published: November 15, 2021 (version 3)

Copyright

© 2021, Sommer et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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  1. Robert A Sommer
  2. Jerry T DeWitt
  3. Raymond Tan
  4. Douglas R Kellogg
(2021)
Growth-dependent signals drive an increase in early G1 cyclin concentration to link cell cycle entry with cell growth
eLife 10:e64364.
https://doi.org/10.7554/eLife.64364

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