scholarly journals Ipl1/Aurora B kinase coordinates synaptonemal complex disassembly with cell cycle progression and crossover formation in budding yeast meiosis

2009 ◽  
Vol 23 (18) ◽  
pp. 2237-2251 ◽  
Author(s):  
P. Jordan ◽  
A. Copsey ◽  
L. Newnham ◽  
E. Kolar ◽  
M. Lichten ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Synaptonemal Complex ◽  
Cell Cycle Progression ◽  
Budding Yeast ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Cycle Progression ◽  
Yeast Meiosis

scholarly journals RecQL4-Aurora B kinase axis is essential for cellular proliferation, cell cycle progression, and mitotic integrity

Oncogenesis ◽  
2018 ◽  
Vol 7 (9) ◽  
Author(s):  
Hongbo Fang ◽  
Kaifeng Niu ◽  
Dongliang Mo ◽  
Yuqi Zhu ◽  
Qunsong Tan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cellular Proliferation ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Cycle Progression

Aurora B kinase is required for cell cycle progression in silkworm

Gene ◽  
2017 ◽  
Vol 599 ◽  
pp. 60-67 ◽  
Author(s):  
Xiaoxu Gang ◽  
Wenliang Qian ◽  
Tianlei Zhang ◽  
Xinxin Yang ◽  
Qingyou Xia ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Cycle Progression

scholarly journals Regulation of Aurora B Expression by the Bromodomain Protein Brd4

2009 ◽  
Vol 29 (18) ◽  
pp. 5094-5103 ◽  
Author(s):  
Jianxin You ◽  
Qing Li ◽  
Chong Wu ◽  
Jina Kim ◽  
Matthias Ottinger ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Chromosome Segregation ◽  
Cell Cycle Progression ◽  
Cellular Proliferation ◽  
Regulatory Gene ◽  
Mitotic Catastrophe ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Cycle Progression

ABSTRACT The bromodomain protein Brd4 plays critical roles in cellular proliferation and cell cycle progression. In this study, we investigated the involvement of Brd4 in cell cycle regulation and observed aberrant chromosome segregation and failures in cytokinesis in cancer cells as well as in primary keratinocytes in which Brd4 has been knocked down by RNA interference. Suppression of Brd4 protein levels in proliferating cells decreased Aurora B protein and transcript levels and abolished its chromosomal distribution. In contrast, exogenous Brd4 expression stimulated Aurora B promoter reporter activity and upregulated endogenous Aurora B expression. Aurora B kinase is a chromosomal passenger protein that is essential for chromosome segregation and cytokinesis. Either overexpression of Aurora B or its inactivation can induce defects in centrosome function, spindle assembly, chromosome alignment, and cytokinesis in various cancer cells. The impaired regulation of Aurora B expression in human cells by Brd4 knockdown or overexpression coincided with mitotic catastrophe and multinucleation that are typically observed when Aurora B is inactivated or overexpressed. Overall, our data suggest that Brd4 is essential for the maintenance of the cell cycle progression mediated at least in part through the control of transcription of the Aurora B kinase cell cycle regulatory gene.

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 Budding Yeast Bub2 Is Localized at Spindle Pole Bodies and Activates the Mitotic Checkpoint via a Different Pathway from Mad2

1999 ◽  
Vol 145 (5) ◽  
pp. 979-991 ◽  
Author(s):  
Roberta Fraschini ◽  
Elisa Formenti ◽  
Giovanna Lucchini ◽  
Simonetta Piatti
Keyword(s):  
Cell Cycle ◽  
Mitotic Spindle ◽  
Cell Cycle Progression ◽  
Budding Yeast ◽  
Spindle Pole Body ◽  
Mitotic Checkpoint ◽  
Spindle Pole ◽  
Cycle Progression ◽  
Spindle Pole Bodies

The mitotic checkpoint blocks cell cycle progression before anaphase in case of mistakes in the alignment of chromosomes on the mitotic spindle. In budding yeast, the Mad1, 2, 3, and Bub1, 2, 3 proteins mediate this arrest. Vertebrate homologues of Mad1, 2, 3, and Bub1, 3 bind to unattached kinetochores and prevent progression through mitosis by inhibiting Cdc20/APC-mediated proteolysis of anaphase inhibitors, like Pds1 and B-type cyclins. We investigated the role of Bub2 in budding yeast mitotic checkpoint. The following observations indicate that Bub2 and Mad1, 2 probably activate the checkpoint via different pathways: (a) unlike the other Mad and Bub proteins, Bub2 localizes at the spindle pole body (SPB) throughout the cell cycle; (b) the effect of concomitant lack of Mad1 or Mad2 and Bub2 is additive, since nocodazole-treated mad1 bub2 and mad2 bub2 double mutants rereplicate DNA more rapidly and efficiently than either single mutant; (c) cell cycle progression of bub2 cells in the presence of nocodazole requires the Cdc26 APC subunit, which, conversely, is not required for mad2 cells in the same conditions. Altogether, our data suggest that activation of the mitotic checkpoint blocks progression through mitosis by independent and partially redundant mechanisms.

scholarly journals Analysis of Cell Cycle Progression in the Budding Yeast S. cerevisiae

2021 ◽  
pp. 265-276
Author(s):  
Deniz Pirincci Ercan ◽  
Frank Uhlmann
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Progression ◽  
Budding Yeast ◽  
Expression Profiles ◽  
Model Organisms ◽  
Cyclin Dependent Kinase ◽  
Cycle Progression ◽  
Daughter Cells ◽  
Substrate Phosphorylation

AbstractThe cell cycle is an ordered series of events by which cells grow and divide to give rise to two daughter cells. In eukaryotes, cyclin–cyclin-dependent kinase (cyclin–Cdk) complexes act as master regulators of the cell division cycle by phosphorylating numerous substrates. Their activity and expression profiles are regulated in time. The budding yeast S. cerevisiae was one of the pioneering model organisms to study the cell cycle. Its genetic amenability continues to make it a favorite model to decipher the principles of how changes in cyclin-Cdk activity translate into the intricate sequence of substrate phosphorylation events that govern the cell cycle. In this chapter, we introduce robust and straightforward methods to analyze cell cycle progression in S. cerevisiae. These techniques can be utilized to describe cell cycle events and to address the effects of perturbations on accurate and timely cell cycle progression.

scholarly journals USP48 Governs Cell Cycle Progression by Regulating the Protein Level of Aurora B

2021 ◽  
Vol 22 (16) ◽  
pp. 8508
Author(s):  
Ainsley Mike Antao ◽  
Kamini Kaushal ◽  
Soumyadip Das ◽  
Vijai Singh ◽  
Bharathi Suresh ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Aurora B ◽  
Deubiquitinating Enzymes ◽  
Cycle Progression ◽  
Protein Levels ◽  
Steady State Levels ◽  
Cycle Regulation ◽  
Normal Cell Cycle

Deubiquitinating enzymes play key roles in the precise modulation of Aurora B—an essential cell cycle regulator. The expression of Aurora B increases before the onset of mitosis and decreases during mitotic exit; an imbalance in these levels has a severe impact on the fate of the cell cycle. Dysregulation of Aurora B can lead to aberrant chromosomal segregation and accumulation of errors during mitosis, eventually resulting in cytokinesis failure. Thus, it is essential to identify the precise regulatory mechanisms that modulate Aurora B levels during the cell division cycle. Using a deubiquitinase knockout strategy, we identified USP48 as an important candidate that can regulate Aurora B protein levels during the normal cell cycle. Here, we report that USP48 interacts with and stabilizes the Aurora B protein. Furthermore, we showed that the deubiquitinating activity of USP48 helps to maintain the steady-state levels of Aurora B protein by regulating its half-life. Finally, USP48 knockout resulted in delayed progression of cell cycle due to accumulation of mitotic defects and ultimately cytokinesis failure, suggesting the role of USP48 in cell cycle regulation.

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