scholarly journals The Molecular Function of the Yeast Polo-like Kinase Cdc5 in Cdc14 Release during Early Anaphase

2009 ◽  
Vol 20 (16) ◽  
pp. 3671-3679 ◽  
Author(s):  
Fengshan Liang ◽  
Fengzhi Jin ◽  
Hong Liu ◽  
Yanchang Wang
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Protein Phosphatase ◽  
Budding Yeast ◽  
Molecular Function ◽  
Cyclin Dependent Kinase ◽  
Yeast Saccharomyces Cerevisiae ◽  
Protein Levels ◽  
Early Anaphase ◽  
Show Evidence ◽  
Mitotic Cyclin

In the budding yeast Saccharomyces cerevisiae , Cdc14 is sequestered within the nucleolus before anaphase entry through its association with Net1/Cfi1, a nucleolar protein. Protein phosphatase PP2ACdc55 dephosphorylates Net1 and keeps it as a hypophosphorylated form before anaphase. Activation of the Cdc fourteen early anaphase release (FEAR) pathway after anaphase entry induces a brief Cdc14 release from the nucleolus. Some of the components in the FEAR pathway, including Esp1, Slk19, and Spo12, inactivate PP2ACdc55, allowing the phosphorylation of Net1 by mitotic cyclin-dependent kinase (Cdk) (Clb2-Cdk1). However, the function of another FEAR component, the Polo-like kinase Cdc5, remains elusive. Here, we show evidence indicating that Cdc5 promotes Cdc14 release primarily by stimulating the degradation of Swe1, the inhibitory kinase for mitotic Cdk. First, we found that deletion of SWE1 partially suppresses the FEAR defects in cdc5 mutants. In contrast, high levels of Swe1 impair FEAR activation. We also demonstrated that the accumulation of Swe1 in cdc5 mutants is responsible for the decreased Net1 phosphorylation. Therefore, we conclude that the down-regulation of Swe1 protein levels by Cdc5 promotes FEAR activation by relieving the inhibition on Clb2-Cdk1, the kinase for Net1 protein.

scholarly journals Separase cooperates with Zds1 and Zds2 to activate Cdc14 phosphatase in early anaphase

2008 ◽  
Vol 182 (5) ◽  
pp. 873-883 ◽  
Author(s):  
Ethel Queralt ◽  
Frank Uhlmann
Keyword(s):  
Cell Cycle ◽  
Budding Yeast ◽  
Mitotic Exit ◽  
Interacting Proteins ◽  
Cyclin Dependent Kinase ◽  
Down Regulation ◽  
Anaphase Onset ◽  
Early Anaphase ◽  
Key Enzyme ◽  
Mitotic Cyclin

Completion of mitotic exit and cytokinesis requires the inactivation of mitotic cyclin-dependent kinase (Cdk) activity. A key enzyme that counteracts Cdk during budding yeast mitotic exit is the Cdc14 phosphatase. Cdc14 is inactive for much of the cell cycle, sequestered by its inhibitor Net1 in the nucleolus. At anaphase onset, separase-dependent down-regulation of PP2ACdc55 allows phosphorylation of Net1 and consequent Cdc14 release. How separase causes PP2ACdc55 down-regulation is not known. Here, we show that two Cdc55-interacting proteins, Zds1 and Zds2, contribute to timely Cdc14 activation during mitotic exit. Zds1 and Zds2 are required downstream of separase to facilitate nucleolar Cdc14 release. Ectopic Zds1 expression in turn is sufficient to down-regulate PP2ACdc55 and promote Net1 phosphorylation. These findings identify Zds1 and Zds2 as new components of the mitotic exit machinery, involved in activation of the Cdc14 phosphatase at anaphase onset. Our results suggest that these proteins may act as separase-regulated PP2ACdc55 inhibitors.

scholarly journals A Late Mitotic Regulatory Network Controlling Cyclin Destruction in Saccharomyces cerevisiae

1998 ◽  
Vol 9 (10) ◽  
pp. 2803-2817 ◽  
Author(s):  
Sue L. Jaspersen ◽  
Julia F. Charles ◽  
Rachel L. Tinker-Kulberg ◽  
David O. Morgan
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Regulatory Network ◽  
Growth Defect ◽  
Cyclin Dependent Kinase ◽  
Anaphase Promoting Complex ◽  
Yeast Saccharomyces Cerevisiae ◽  
Mitotic Cyclin ◽  
Low Levels ◽  
Late Mitosis ◽  
Mutant Cells

Exit from mitosis requires the inactivation of mitotic cyclin-dependent kinase–cyclin complexes, primarily by ubiquitin-dependent cyclin proteolysis. Cyclin destruction is regulated by a ubiquitin ligase known as the anaphase-promoting complex (APC). In the budding yeast Saccharomyces cerevisiae, members of a large class of late mitotic mutants, including cdc15,cdc5, cdc14, dbf2, andtem1, arrest in anaphase with a phenotype similar to that of cells expressing nondegradable forms of mitotic cyclins. We addressed the possibility that the products of these genes are components of a regulatory network that governs cyclin proteolysis. We identified a complex array of genetic interactions among these mutants and found that the growth defect in most of the mutants is suppressed by overexpression of SPO12, YAK1, andSIC1 and is exacerbated by overproduction of the mitotic cyclin Clb2. When arrested in late mitosis, the mutants exhibit a defect in cyclin-specific APC activity that is accompanied by high Clb2 levels and low levels of the anaphase inhibitor Pds1. Mutant cells arrested in G1 contain normal APC activity. We conclude that Cdc15, Cdc5, Cdc14, Dbf2, and Tem1 cooperate in the activation of the APC in late mitosis but are not required for maintenance of that activity in G1.

scholarly journals Novel E3 Ubiquitin Ligases That Regulate Histone Protein Levels in the Budding Yeast Saccharomyces cerevisiae

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e36295 ◽  
Author(s):  
Rakesh Kumar Singh ◽  
Melanie Gonzalez ◽  
Marie-Helene Miquel Kabbaj ◽  
Akash Gunjan
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Budding Yeast ◽  
Ubiquitin Ligases ◽  
E3 Ubiquitin Ligases ◽  
Yeast Saccharomyces Cerevisiae ◽  
Histone Protein ◽  
Protein Levels

scholarly journals Filamentous growth of the budding yeast Saccharomyces cerevisiae induced by overexpression of the WHI2 gene

Microbiology ◽  
1997 ◽  
Vol 143 (6) ◽  
pp. 1867-1876 ◽  
Author(s):  
P. A. Radcliffe ◽  
K. M. Binley ◽  
J. Trevethick ◽  
M. Hall ◽  
P. E. Sudbery
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Budding Yeast ◽  
Filamentous Growth ◽  
Yeast Saccharomyces Cerevisiae

scholarly journals Budding yeast relies on G1 cyclin specificity to couple cell cycle progression with morphogenetic development

2021 ◽  
Vol 7 (23) ◽  
pp. eabg0007
Author(s):  
Deniz Pirincci Ercan ◽  
Florine Chrétien ◽  
Probir Chakravarty ◽  
Helen R. Flynn ◽  
Ambrosius P. Snijders ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Budding Yeast ◽  
Quantitative Model ◽  
Cyclin Dependent Kinase ◽  
Cycle Progression ◽  
Model Cell ◽  
Mitotic Cyclin ◽  
Substrate Phosphorylation ◽  
The Cost

Two models have been put forward for cyclin-dependent kinase (Cdk) control of the cell cycle. In the qualitative model, cell cycle events are ordered by distinct substrate specificities of successive cyclin waves. Alternatively, in the quantitative model, the gradual rise of Cdk activity from G1 phase to mitosis leads to ordered substrate phosphorylation at sequential thresholds. Here, we study the relative contributions of qualitative and quantitative Cdk control in Saccharomyces cerevisiae. All S phase and mitotic cyclins can be replaced by a single mitotic cyclin, albeit at the cost of reduced fitness. A single cyclin can also replace all G1 cyclins to support ordered cell cycle progression, fulfilling key predictions of the quantitative model. However, single-cyclin cells fail to polarize or grow buds and thus cannot survive. Our results suggest that budding yeast has become dependent on G1 cyclin specificity to couple cell cycle progression to essential morphogenetic events.

scholarly journals Systems Level Modeling of the Cell Cycle Using Budding Yeast

2007 ◽  
Vol 3 ◽  
pp. 117693510700300 ◽  
Author(s):  
B.P. Ingalls ◽  
B.P. Duncker ◽  
D.R. Kim ◽  
B.J. McConkey
Keyword(s):  
Cell Cycle ◽  
Budding Yeast ◽  
Human Cancer ◽  
Quality Data ◽  
Cell Cycle Gene ◽  
Mathematical Framework ◽  
Gene Transcript ◽  
Proteomics Data ◽  
Yeast Saccharomyces Cerevisiae ◽  
Protein Levels

Proteins involved in the regulation of the cell cycle are highly conserved across all eukaryotes, and so a relatively simple eukaryote such as yeast can provide insight into a variety of cell cycle perturbations including those that occur in human cancer. To date, the budding yeast Saccharomyces cerevisiae has provided the largest amount of experimental and modeling data on the progression of the cell cycle, making it a logical choice for in-depth studies of this process. Moreover, the advent of methods for collection of high-throughput genome, transcriptome, and proteome data has provided a means to collect and precisely quantify simultaneous cell cycle gene transcript and protein levels, permitting modeling of the cell cycle on the systems level. With the appropriate mathematical framework and sufficient and accurate data on cell cycle components, it should be possible to create a model of the cell cycle that not only effectively describes its operation, but can also predict responses to perturbations such as variation in protein levels and responses to external stimuli including targeted inhibition by drugs. In this review, we summarize existing data on the yeast cell cycle, proteomics technologies for quantifying cell cycle proteins, and the mathematical frameworks that can integrate this data into representative and effective models. Systems level modeling of the cell cycle will require the integration of high-quality data with the appropriate mathematical framework, which can currently be attained through the combination of dynamic modeling based on proteomics data and using yeast as a model organism.

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