Fission yeast cut5+, required for S phase onset and M phase restraint, is identical to the radiation-damage repair gene rad4+

Yasushi Saka, M Yanagida

Research output: Contribution to journalArticle

193 Citations (Scopus)

Abstract

Fission yeast cut5 mutants cause cytokinesis in the absence of normal nuclear division. We show here that cut5+ is required for both the onset of S phase and the restraint of M phase before the completion of S phase. The primary defects in cut5 mutants occur prior to S phase, but cells suffer lethal damage during M phase. Mitosis and cytokinesis occur in the presence of hydroxyurea or in the double mutant cdc10-cut5 (the cdc10 mutation alone blocks progression from G1 to S). Gene cloning shows that cut5+ is identical to the fission yeast rad4+ gene, which is similar to human XRCC1. The rad4+/cut5+ gene is unique in its positive role for replication/repair and in its negative role for mitosis/cytokinesis. We propose a single/twin chromatid marking model for rad4+/cut5+ function in cell cycle control.
Original languageEnglish
Pages (from-to)383-393
Number of pages11
JournalCell
Volume74
Issue number2
DOIs
Publication statusPublished - 30 Jul 1993

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Cytokinesis
Schizosaccharomyces
Radiation damage
S Phase
Cell Division
Yeast
Repair
Genes
Radiation
Mitosis
Cell Nucleus Division
Chromatids
Hydroxyurea
Cloning
Cell Cycle Checkpoints
Organism Cloning
Cells
Defects
Mutation

Keywords

  • Amino Acid Sequence
  • Base Sequence
  • Cell Cycle
  • Cell Cycle Proteins
  • Cell Division
  • Cell Nucleus
  • Cloning, Molecular
  • DNA, Fungal
  • DNA-Binding Proteins
  • Fungal Proteins
  • Genes, Fungal
  • Mitosis
  • Models, Genetic
  • Molecular Sequence Data
  • Nitrogen
  • Phenotype
  • S Phase
  • Schizosaccharomyces
  • Schizosaccharomyces pombe Proteins
  • Transcription Factors
  • Transformation, Genetic
  • Transglutaminases
  • Ultraviolet Rays
  • X-Rays

Cite this

Fission yeast cut5+, required for S phase onset and M phase restraint, is identical to the radiation-damage repair gene rad4+. / Saka, Yasushi; Yanagida, M.

In: Cell, Vol. 74, No. 2, 30.07.1993, p. 383-393.

Research output: Contribution to journalArticle

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abstract = "Fission yeast cut5 mutants cause cytokinesis in the absence of normal nuclear division. We show here that cut5+ is required for both the onset of S phase and the restraint of M phase before the completion of S phase. The primary defects in cut5 mutants occur prior to S phase, but cells suffer lethal damage during M phase. Mitosis and cytokinesis occur in the presence of hydroxyurea or in the double mutant cdc10-cut5 (the cdc10 mutation alone blocks progression from G1 to S). Gene cloning shows that cut5+ is identical to the fission yeast rad4+ gene, which is similar to human XRCC1. The rad4+/cut5+ gene is unique in its positive role for replication/repair and in its negative role for mitosis/cytokinesis. We propose a single/twin chromatid marking model for rad4+/cut5+ function in cell cycle control.",
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N2 - Fission yeast cut5 mutants cause cytokinesis in the absence of normal nuclear division. We show here that cut5+ is required for both the onset of S phase and the restraint of M phase before the completion of S phase. The primary defects in cut5 mutants occur prior to S phase, but cells suffer lethal damage during M phase. Mitosis and cytokinesis occur in the presence of hydroxyurea or in the double mutant cdc10-cut5 (the cdc10 mutation alone blocks progression from G1 to S). Gene cloning shows that cut5+ is identical to the fission yeast rad4+ gene, which is similar to human XRCC1. The rad4+/cut5+ gene is unique in its positive role for replication/repair and in its negative role for mitosis/cytokinesis. We propose a single/twin chromatid marking model for rad4+/cut5+ function in cell cycle control.

AB - Fission yeast cut5 mutants cause cytokinesis in the absence of normal nuclear division. We show here that cut5+ is required for both the onset of S phase and the restraint of M phase before the completion of S phase. The primary defects in cut5 mutants occur prior to S phase, but cells suffer lethal damage during M phase. Mitosis and cytokinesis occur in the presence of hydroxyurea or in the double mutant cdc10-cut5 (the cdc10 mutation alone blocks progression from G1 to S). Gene cloning shows that cut5+ is identical to the fission yeast rad4+ gene, which is similar to human XRCC1. The rad4+/cut5+ gene is unique in its positive role for replication/repair and in its negative role for mitosis/cytokinesis. We propose a single/twin chromatid marking model for rad4+/cut5+ function in cell cycle control.

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