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Shrinking Daughters: Rlm1-Dependent G1/S Checkpoint Maintains Saccharomyces cerevisiae Daughter Cell Size and
Sarah Piccirillo1, Deepshikha Neog1, David Spade2
1Division of Cell Biology and Biophysics, University of Missouri-Kansas City, Missouri 64110.
Genetics
|June 23, 2017
Summary
The Rlm1 protein acts as a cell wall/START (CW/START) checkpoint, delaying cell division. Deleting Rlm1 causes cells to form satellite daughters that cannot divide, revealing Rlm1
Area of Science:
- Cell biology
- Molecular biology
- Yeast genetics
Background:
- The Rlm1 transcription factor is integral to the cell wall integrity pathway in yeast.
- Cell cycle progression is tightly regulated by various internal and external cues.
Purpose of the Study:
- To investigate the role of the Rlm1 transcription factor in cell cycle regulation.
- To elucidate the mechanism of the cell wall/START (CW/START) checkpoint.
Main Methods:
- Generating and analyzing an rlm1Δ mutant yeast strain.
- Observing cell morphology and division patterns under specific growth conditions (nonfermentable carbon source, low osmolarity).
- Utilizing genetic manipulation (gene deletion) and UV irradiation to assess cell cycle progression and rescue phenotypes.
Main Results:
- rlm1Δ mutants formed unique cell aggregates with a mother cell surrounded by smaller satellite daughters.
- Mother cells in rlm1Δ mutants initiated cell division prematurely (precocious START).
- Satellite daughters exhibited impaired growth and division, even after transfer to rich media, suggesting a defect in cell cycle re-entry.
Conclusions:
- Rlm1 acts as a crucial regulator, delaying the G1 to S phase transition, establishing the CW/START checkpoint.
- The Slt2 kinase and Swi4 protein are involved in regulating the START transition, with Slt2 potentially having opposing roles.
- Proper duplication of the actin-organizing center in late G1 is hypothesized to be essential for both START progression and daughter cell actin cytoskeleton establishment.
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