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Efficient Sporulation of Saccharomyces cerevisiae in a 96 Multiwell Format
Published on: September 17, 2016
Morphogenesis beyond cytokinetic arrest in Saccharomyces cerevisiae
The Journal of Cell Biology
|December 16, 1998
Summary
The budding yeast cdc15 mutation causes cell lysis by preventing proper cell division. This study reveals a checkpoint linking cell cycle initiation to the completion of cytokinesis, crucial for yeast cell survival.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- The lyt1 mutation in budding yeast leads to cell lysis.
- cdc15 is a gene encoding a protein kinase involved in late cell cycle progression.
Purpose of the Study:
- To investigate the function of the cdc15 gene and its role in cell cycle progression and cytokinesis.
- To elucidate the cause of cell lysis observed in cdc15 mutants.
Main Methods:
- Genetic analysis of yeast mutants (lyt1, cdc15, bud1, cdc28, CDC14, DBF2, TEM1, septin mutants).
- Microscopy to observe cell morphology, actin polarization, and septin localization.
- Cell cycle analysis including DNA replication and budding.
Main Results:
- cdc15 and cdc15-lyt1 mutants fail to septate at 37°C and exhibit cell lysis after forming shmoo-like projections.
- Actin polarization occurs at the distal pole, while septins remain at the mother-daughter neck.
- Mutations in functionally related genes (CDC14, DBF2, TEM1) cause similar phenotypes.
- Apical polarization is delayed in cdc15 mutants, a delay abolished in septin mutants.
Conclusions:
- The delayed M/G1 transition in cdc15 mutants is caused by a checkpoint that couples cell cycle initiation to cytokinesis completion.
- Septin function is critical for this checkpoint, ensuring proper cell division and preventing lysis.
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