G1 Cyclins Block the Ime1 Pathway to Make Mitosis and Meiosis Incompatible in Budding Yeast

EMBO J. 1999 Jan 15;18(2):320-9. doi: 10.1093/emboj/18.2.320.

Abstract

Diploid yeast cells switch from mitosis to meiosis when starved of essential nutrients. While G1 cyclins play a key role in initiating the mitotic cell cycle, entry into meiosis depends on Ime1, a transcriptional activator regulated by both nutritional and cell-type signals. We show here that G1 cyclins downregulate IME1 transcription and prevent the accumulation of the Ime1 protein within the nucleus, which results in repression of early-meiotic gene expression. As G1-cyclin deficient cells do not require nutrient starvation to undergo meiosis, G1 cyclin would exert its role by transmitting essential nutritional signals to Ime1 function. The existence of a negative cross-talk mechanism between mitosis and meiosis may help explain why these two developmental options are incompatible in budding yeast.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Nucleus / physiology
  • Culture Media
  • Cyclins / genetics
  • Cyclins / physiology*
  • Fungal Proteins / genetics
  • Fungal Proteins / physiology*
  • G1 Phase / genetics
  • G1 Phase / physiology*
  • Gene Expression
  • Genes, Fungal
  • Meiosis / genetics
  • Meiosis / physiology*
  • Mitosis / genetics
  • Mitosis / physiology*
  • Nuclear Proteins / genetics
  • Nuclear Proteins / physiology*
  • S Phase / genetics
  • S Phase / physiology
  • Saccharomyces cerevisiae / cytology*
  • Saccharomyces cerevisiae / genetics
  • Saccharomyces cerevisiae / physiology*
  • Saccharomyces cerevisiae Proteins*
  • Signal Transduction
  • Trans-Activators / genetics
  • Trans-Activators / physiology
  • Transcription Factors*

Substances

  • CLN1 protein, S cerevisiae
  • CLN2 protein, S cerevisiae
  • CLN3 protein, S cerevisiae
  • Culture Media
  • Cyclins
  • Fungal Proteins
  • IME1 protein, S cerevisiae
  • Nuclear Proteins
  • Saccharomyces cerevisiae Proteins
  • Trans-Activators
  • Transcription Factors