Functions of the mitotic B-type cyclins CLB1, CLB2, and CLB3 at mitotic exit antagonized by the CDC14 phosphatase

Tzeng, Yao-Wei; Huang, James N.; Schuyler, Scott C.; Wu, Chun-Hao; Juang, Yue‐Li

doi:10.1016/j.fgb.2011.07.001

Cited by 6 publications

(5 citation statements)

References 46 publications

(64 reference statements)

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“…Supporting this vision, recent analyses reveal a different function for Clb1, Clb2 and Clb3 at mitotic exit, and are consistent with the hypothesis that Clbassociated functions are antagonized by Cdc14 to couple cell cycle progression with cytokinesis at mitotic exit [160]. The specific functions of Clb cyclins during cell cycle progression and cytokinesis have been investigated, revealing that: (a) Clb1 inactivation mainly inhibits cell cycle progression, with less influence on the inactivation of Clb2 or Clb3, (b) Clb2 inactivation is involved in the formation of the actin ring structure and (c) inactivation of both Clb1 and Clb3 is sufficient to complete cytokinesis and therefore cell division, with an additional effect of Clb3 in promoting polarized growth [160]. These data are in agreement with early evidence showing that Clb2 and Clb5 differ strikingly in the cell cycle events that they can drive efficiently, even when present at similar levels and at similar times [155].…”

Section: Have We Discovered All Regulatory Functions Of Sic1?supporting

confidence: 76%

“…It has been shown that the balance between Cdk1 ⁄ Clb2 and Cdc14 is critical for proper regulation at mitotic exit [158] and that the balance between oscillating Cdk1 ⁄ Clb activity and the execution of Cdc14 functions is central in the regulation of cell cycle progression at mitotic exit [159]. Supporting this vision, recent analyses reveal a different function for Clb1, Clb2 and Clb3 at mitotic exit, and are consistent with the hypothesis that Clbassociated functions are antagonized by Cdc14 to couple cell cycle progression with cytokinesis at mitotic exit [160]. The specific functions of Clb cyclins during cell cycle progression and cytokinesis have been investigated, revealing that: (a) Clb1 inactivation mainly inhibits cell cycle progression, with less influence on the inactivation of Clb2 or Clb3, (b) Clb2 inactivation is involved in the formation of the actin ring structure and (c) inactivation of both Clb1 and Clb3 is sufficient to complete cytokinesis and therefore cell division, with an additional effect of Clb3 in promoting polarized growth [160].…”

Section: Have We Discovered All Regulatory Functions Of Sic1?supporting

confidence: 68%

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Sic1 as a timer of Clb cyclin waves in the yeast cell cycle – design principle of not just an inhibitor

Barberis

2012

The FEBS Journal

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Cellular systems biology aims to uncover design principles that describe the properties of biological networks through interaction of their components in space and time. The cell cycle is a complex system regulated by molecules that are integrated into functional modules to ensure genome integrity and faithful cell division. In budding yeast, cyclin-dependent kinases (Cdk1/Clb) drive cell cycle progression, being activated and inactivated in a precise temporal sequence. In this module, which we refer to as the 'Clb module', different Cdk1/Clb complexes are regulated to generate waves of Clb activity, a functional property of cell cycle control. The inhibitor Sic1 plays a critical role in the Clb module by binding to and blocking Cdk1/Clb activity, ultimately setting the timing of DNA replication and mitosis. Fifteen years of research subsequent to the identification of Sic1 have lead to the development of an integrative approach that addresses its role in regulating the Clb module. Sic1 is an intrinsically disordered protein and achieves its inhibitory function by cooperative binding, where different structural regions stretch on the Cdk1/Clb surface. Moreover, Sic1 promotes S phase entry, facilitating Cdk1/Clb5 nuclear transport, and therefore revealing a double function of inhibitor/activator that rationalizes a mechanism to prevent precocious DNA replication. Interestingly, the investigation of Clb temporal dynamics by mathematical modelling and experimental validation provides evidence that Sic1 acts as a timer to coordinate oscillations of Clb cyclin waves. Here we review these findings, focusing on the design principle underlying the Clb module, which highlights the role of Sic1 in regulating phase-specific Cdk1/Clb activities.

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Section: Have We Discovered All Regulatory Functions Of Sic1?supporting

confidence: 76%

Section: Have We Discovered All Regulatory Functions Of Sic1?supporting

confidence: 68%

Sic1 as a timer of Clb cyclin waves in the yeast cell cycle – design principle of not just an inhibitor

Barberis

2012

The FEBS Journal

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“…The conjoint action of Hsl1p and Gin4p, as well as the inactivation of Swe1p, drives the septin formation, which in turn, prompts the M phase entry by a synergic action with the Clb1/2p activation (Barral et al 1999; Asano et al 2006). The action of Clb1/2p holds cells at the end of the M phase, then the complete inhibition of this protein is required for the M phase release (Tzeng et al 2011). Our modeling inhibition of Hsl1P and Gin4p by lnc9136 positively impacts the Swe1p (which inhibits the Clb1/2p) peaking to an M phase release and the cell cycle restart.…”

Section: Discussionmentioning

confidence: 99%

LncRNAs of Saccharomyces cerevisiae dodge the cell cycle arrest imposed by the ethanol stress

et al. 2021

Preprint

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Ethanol impairs many subsystems of Saccharomyces cerevisiae, including the cell cycle. Cyclins and damage checkpoints drive the cell cycle. Two ethanol-responsive lncRNAs in yeast interact with cell cycle proteins, and here we investigated the role of these RNAs on the ethanol-stressed cell cycle. Our network dynamic modeling showed that the higher and lower ethanol tolerant strains undergo a cell cycle arrest during the ethanol stress. However, lower tolerant phenotype arrest in a later phase leading to its faster population rebound after the stress relief. Two lncRNAs can skip the arrests mentioned. The in silico overexpression of lnc9136 of SEY6210 (a lower tolerant strain), and CRISPR-Cas9 partial deletions of this lncRNA, evidenced that the one induces a regular cell cycle even under ethanol stress; this lncRNA binds to Gin4 and Hsl1, driving the Swe1p, Clb1/2, and cell cycle. Moreover, the lnc10883 of BY4742 (a higher tolerant strain) interacts to the Mec1p and represses Bub1p, circumventing the DNA and spindle damage checkpoints keeping a normal cell cycle even under DNA damage. Overall, we present the first evidence of the direct roles of lncRNAs on cell cycle proteins, the dynamics of this system in different ethanol tolerant phenotypes, and a new cell cycle model.

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“…Clb1/2p halts cells at the end of M phase. Therefore, the M phase exit relies on Clb1/2p inhibition [64]. Cdc20p (represented by APCC_Cdc20 in our model) is essential for APC/C [65] and suffices for mitotic exit in yeast by degrading Clb2p [66].…”

Section: The Lncrna Lnc9136 Prevents Cell Cycle Arrest In Strain Sey6...mentioning

confidence: 99%

LncRNAs of Saccharomyces cerevisiae bypass the cell cycle arrest imposed by ethanol stress

et al. 2022

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Ethanol alters many subsystems of Saccharomyces cerevisiae, including the cell cycle. Two ethanol-responsive lncRNAs in yeast interact with cell cycle proteins, and here, we investigated the role of these RNAs in cell cycle. Our network dynamic modeling showed that higher and lower ethanol-tolerant strains undergo cell cycle arrest in mitosis and G1 phases, respectively, during ethanol stress. The higher population rebound of the lower ethanol-tolerant phenotype after stress relief responds to the late phase arrest. We found that the lncRNA lnc9136 of SEY6210 (a lower ethanol-tolerant strain) induces cells to skip mitosis arrest. Simulating an overexpression of lnc9136 and analyzing CRISPR–Cas9 mutants lacking this lncRNA suggest that lnc9136 induces a regular cell cycle even under ethanol stress, indirectly regulating Swe1p and Clb1/2 by binding to Gin4p and Hsl1p. Notably, lnc10883 of BY4742 (a higher ethanol-tolerant strain) does not prevent G1 arrest in this strain under ethanol stress. However, lnc19883 circumvents DNA and spindle damage checkpoints, maintaining a functional cell cycle by interacting with Mec1p or Bub1p even in the presence of DNA/spindle damage. Overall, we present the first evidence of direct roles for lncRNAs in regulating yeast cell cycle proteins, the dynamics of this system in different ethanol-tolerant phenotypes, and a new yeast cell cycle model.

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Functions of the mitotic B-type cyclins CLB1, CLB2, and CLB3 at mitotic exit antagonized by the CDC14 phosphatase

Cited by 6 publications

References 46 publications

Sic1 as a timer of Clb cyclin waves in the yeast cell cycle – design principle of not just an inhibitor

Sic1 as a timer of Clb cyclin waves in the yeast cell cycle – design principle of not just an inhibitor

LncRNAs of Saccharomyces cerevisiae dodge the cell cycle arrest imposed by the ethanol stress

LncRNAs of Saccharomyces cerevisiae bypass the cell cycle arrest imposed by ethanol stress

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