Coupling of cell division to cell growth by translational control of the G1 cyclin CLN3 in yeast

  1. Michael Polymenis1 and
  2. Emmett V. Schmidt1,2,3
  1. 1MGH Cancer Center, Massachusetts General Hospital, Charlestown, Massachusetts 02129 USA; 2The Pediatric Service, Massachusetts General Hospital, and the Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02114 USA

Abstract

The eukaryotic cell cycle is driven by a cascade of cyclins and kinase partners including the G1 cyclin Cln3p in yeast. As the first step in this cascade, Cln3p is uniquely positioned to determine the critical growth-rate threshold for division. To analyze factors regulating CLN3 expression, we identified a short upstream open reading frame (uORF) in the 5′ leader of CLN3mRNA as a translational control element. This control element is critical for the growth-dependent regulation of Cln3p synthesis because it specifically represses CLN3 expression during conditions of diminished protein synthesis or slow growth. Inactivation of the uORF accelerates the completion of Start and entry into the cell cycle suggesting that translational regulation of CLN3 provides a mechanism coupling cell growth and division.

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Footnotes

  • 3 Corresponding author.

  • E-MAIL schmidt{at}helix.mgh.harvard.edu; FAX (617) 726-5637.

    • Received July 10, 1997.
    • Accepted August 11, 1997.
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