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Cell cycle control of septin ring dynamics in the budding yeast
Vı Ctor J Cid1, Lubica Adamiková2, Miguel Sánchez3
1Departamento de Microbiologı́a II, Facultad de Farmacia, Universidad Complutense, 28040-Madrid, Spain1.
This study explores how cell cycle signals control septin ring dynamics in budding yeast. Septins form a ring that marks the site of cell division and helps regulate cell shape and growth. The researchers found that septin ring assembly depends on G1 cyclins and the GTPase Cdc42. During bud growth, the ring remains stable even when mitotic checkpoints are disrupted. At the end of the cell cycle, the ring splits into two structures, a process that requires the mitotic exit network and the Cdc14 phosphatase. The study shows that cell cycle signals are essential for coordinating septin behavior with cell division and morphogenesis.
Area of Science:
- Cell cycle regulation in fungal biology
- Cytoskeletal dynamics in yeast morphogenesis
- Molecular mechanisms of cell division
Background:
Septins are cytoskeletal proteins found in eukaryotes, playing roles in cell division and morphogenesis. In budding yeast, they form a ring structure at the site of cell division. Prior research has shown that septins contribute to cell polarity and chitin synthesis. However, the precise regulation of septin dynamics during the cell cycle remains unclear. This gap motivated the investigation of how cell cycle signals influence septin behavior. No prior work had resolved how septin assembly depends on specific cyclins or GTPases. Understanding these mechanisms could clarify how morphogenesis is coordinated with cell division. The study aimed to address this uncertainty by examining septin ring dynamics in synchronized yeast cells. The focus was on how cell cycle checkpoints and regulatory proteins affect septin structure formation and disassembly.
Purpose Of The Study:
The study aimed to investigate how cell cycle signals regulate septin ring dynamics in budding yeast. Specifically, the researchers sought to determine whether septin assembly depends on G1 cyclins and Cdc42. They also wanted to assess how septin structures respond to disruptions in mitotic regulation. The motivation was to clarify the role of cell cycle checkpoints in morphogenesis. By using time-lapse confocal microscopy, the team could track septin behavior in live cells. The study focused on how septin rings form and disassemble during the cell cycle. The goal was to identify which cell cycle regulators are essential for septin function. This approach allowed the researchers to link cytoskeletal dynamics to cell cycle progression.
Main Methods:
The researchers used a septin-GFP fusion to visualize septin structures in live yeast cells. Time-lapse confocal microscopy was employed to track septin ring dynamics during the cell cycle. Specific cell cycle arrests were induced to test the effects of G1 cyclins and Cdc42. The team also examined the impact of DNA repair and spindle assembly checkpoints on septin behavior. They analyzed septin ring duplication and splitting during late mitosis. The study included pseudohyphal growth and budding zygotes to observe septin dynamics in different contexts. The role of the mitotic exit network was assessed by monitoring Cdc14 phosphatase activity. These methods allowed the researchers to correlate septin behavior with cell cycle regulation.
Main Results:
Septin ring assembly was found to depend on G1 cyclin/Cdc28 signaling and Cdc42 activity. The ring remained stable during bud growth, even when mitotic checkpoints were disrupted. Septin structures duplicated at late mitosis and split after cell separation. The mitotic exit network, including Cdc14, was essential for ring splitting. Septin dynamics were unaffected by DNA repair or spindle assembly checkpoint failures. The ring spanned the bud neck and was maintained during bud emergence. The study showed that septin ring formation is independent of Rho1. These findings suggest that cell cycle signals regulate septin behavior to coordinate morphogenesis.
Conclusions:
The study supports a role for cell cycle control in regulating septin dynamics. Septin ring assembly depends on G1 cyclins and Cdc42, as stated by the authors. The ring remains stable during bud growth despite mitotic disruptions. The mitotic exit network is essential for ring splitting, according to the authors. Septin structures are unaffected by DNA repair or spindle checkpoint failures. The authors propose that septin dynamics are coordinated with cell cycle progression. These findings suggest that septin behavior is tightly regulated to ensure proper morphogenesis. The authors conclude that cell cycle signals are necessary for accurate septin function.
Frequently Asked Questions
Septin rings mark the cytokinetic plane and regulate morphogenesis, including chitin synthesis and bud growth.
The small GTPase Cdc42 is essential for septin ring assembly, but Rho1 is not.
The mitotic exit network, including Cdc14, is required for splitting the septin ring into two structures after cell separation.
No, septin ring dynamics remain unaffected by DNA repair or spindle assembly checkpoint failures.
The ring spans the bud neck and remains stable during bud growth, even when mitotic checkpoints are disrupted.
The authors propose that G1 cyclin/Cdc28-mediated signals are essential for septin ring assembly.