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Cdc28 tyrosine phosphorylation and the morphogenesis checkpoint in budding yeast
1Department of Molecular Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Molecular Biology of the Cell
|November 1, 1996
Summary
The budding yeast morphogenesis checkpoint delays cell division when cells fail to bud, requiring the SWE1 gene. This checkpoint primarily uses post-translational regulation of Swe1, not just mRNA levels, to delay nuclear division.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- A morphogenesis checkpoint in budding yeast delays nuclear division when bud formation fails.
- This checkpoint is crucial for cell cycle progression and proper cell division.
Purpose of the Study:
- To investigate the molecular mechanisms underlying the morphogenesis checkpoint in budding yeast.
- To determine the role of the SWE1 gene and Cdc28 phosphorylation in this checkpoint.
Main Methods:
- Genetic analysis of SWE1 and MIH1 gene dosage.
- Analysis of Cdc28 phosphorylation at tyrosine 19.
- Monitoring of SWE1 mRNA levels during the cell cycle.
- Investigating checkpoint function under deregulated SWE1 transcription.
Main Results:
- The SWE1 gene is essential for the morphogenesis checkpoint to delay nuclear division.
- Cdc28 phosphorylation at tyrosine 19 is critical for timing nuclear division in unbudded cells.
- SWE1 mRNA levels fluctuate and are elevated in unbudded cells, but checkpoint regulation is indirect.
- The checkpoint can delay nuclear division even with deregulated SWE1 transcription, suggesting post-translational control.
Conclusions:
- The morphogenesis checkpoint delays nuclear division primarily through post-translational regulation of the Swe1 kinase.
- Transcriptional feedback loops involving SWE1 enhance the checkpoint's effectiveness.
- Understanding this checkpoint provides insights into cell cycle regulation and morphogenesis.