Mutational analysis of Cak1p, an essential protein kinase that regulates cell cycle progression

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

In Saccharomyces cerevisiae, entry into S phase requires the activation of the proteinkinase Cdc28p through binding with cyclin Clb5p or Clb6p, as well as the destruction of the cyclin-dependent kinase inhibitor Sic1p. Mutants that are defective in this activation event arrest after START, with unreplicated DNA and multiple, elongated buds. These mutants include cells defective in CDC4, CDC34 or CDC53, as well as cells that have lost all CLB function. Here we describe mutations in another gene, CAK1, that lead to a similar arrest. Cells that are defective in CAK1 are inviable and arrest with a single nucleus and multiple, elongated buds. CAK1 encodes a protein kinase most closely related to the Cdc2p family of protein kinases. Mutations that lead to the production of an inactive kinase that call neither autophosphorylate, nor phosphorylate Cdc28p in vitro are also incapable of rescuing a cell with a deletion of CAK1. These results underscore the importance of the Cak1p protein kinase activity in cell cycle progression.

Original languageEnglish (US)
Pages (from-to)365-375
Number of pages11
JournalMolecular and General Genetics
Volume256
Issue number4
DOIs
StatePublished - Nov 27 1997

Keywords

  • CAK
  • Cell cycle
  • Cyclin-dependent kinase
  • Elongated buds
  • Protein kinase

ASJC Scopus subject areas

  • Genetics

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