scholarly journals Genome-wide analysis of cell cycle-regulating genes in the symbiotic dinoflagellate Symbiodinium minutum

2018 ◽  
Author(s):  
Michael L. Cato ◽  
Hallie D. Jester ◽  
Adam Lavertu ◽  
Audrey Lyman ◽  
Lacey M. Tallent ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Molecular Mechanisms ◽  
Algal Cell ◽  
Cycle Phase ◽  
Symbiotic Dinoflagellate ◽  
Cyclin Dependent Kinases ◽  
Cell Divisions ◽  
Genome Wide ◽  
Summer Maximum ◽  
Reef Health

ABSTRACTA critical relationship exists between reef-building corals and their photosynthetic endosymbionts. As important as this relationship is for reef health, it is exquisitely delicate—exposure to temperatures only marginally above the average summer maximum can cause corals to bleach, expelling their resident algae. Interestingly, several studies indicate that failure of corals to properly regulate symbiont cell divisions at high temperatures may cause bleaching. This needs to be further investigated, but first, it is necessary to decipher the molecular mechanisms controlingl the cell division cycle in these organisms. As a first step toward this goal, we identified key cell cycle-regulating genes in the recently published genome of the symbiotic dinoflagellate Symbiodinium minutum. We then correlated expression of these genes with cell cycle phase in diurnally growing S. minutum in culture. Of particular interest, this approach allowed us to identify cyclins and cyclin-dependent kinases that are involved in the G1/S transition—a likely point for coral cells to exert control over algal cell divisions.

DNA damage inhibits proteolysis of the B-type cyclin Clb5 in S. cerevisiae

1997 ◽  
Vol 110 (15) ◽  
pp. 1813-1820
Author(s):  
D. Germain ◽  
J. Hendley ◽  
B. Futcher
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Tyrosine Phosphorylation ◽  
Cell Cycle Progression ◽  
Cycle Phase ◽  
Cycle Progression ◽  
Ubiquitin Pathway ◽  
Cyclin Dependent Kinases ◽  
Transition Points ◽  
Checkpoint Genes

Cell cycle progression is mediated by waves of specific cyclin dependent kinases (CDKs) in all eukaryotes. Cyclins are degraded by the ubiquitin pathway of proteolysis. The recent identification of several components of the cyclin proteolysis machinery has highlighted both the importance of proteolysis at multiple transition points in the cell cycle and the involvement of other substrates degraded by the same machinery. In this study, we have investigated the effects of DNA damage on the cyclin proteolytic machinery in Saccharomyces cerevisiae. We find that the half-life of the B-type cyclin Clb5 is markedly increased following DNA damage while that of G1 cyclins is not. This effect is independent of cell cycle phase. Clb5 turnover requires p34CDC28 activity. Stabilisation of Clb5 correlates with an increase in tyrosine phosphorylation of p34CDC28, but stabilisation does not require this tyrosine phosphorylation. The stabilisation is independent of the checkpoint genes Mec1 and Rad53. These observations establish a new link between the regulation of proteolysis and DNA damage.

scholarly journals Plant CDKs—Driving the Cell Cycle through Climate Change

Plants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1804
Author(s):  
Aline Köhn Carneiro ◽  
Patrícia da Fonseca Montessoro ◽  
Adriana Flores Fusaro ◽  
Bruna Gino Araújo ◽  
Adriana Silva Hemerly
Keyword(s):  
Climate Change ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Primary Response ◽  
Environmental Response ◽  
Adaptive Responses ◽  
Climate Fluctuations ◽  
Cyclin Dependent Kinases ◽  
Cell Divisions ◽  
The Face

In a growing population, producing enough food has become a challenge in the face of the dramatic increase in climate change. Plants, during their evolution as sessile organisms, developed countless mechanisms to better adapt to the environment and its fluctuations. One important way is through the plasticity of their body and their forms, which are modulated during plant growth by accurate control of cell divisions. A family of serine/threonine kinases called cyclin-dependent kinases (CDK) is a key regulator of cell divisions by controlling cell cycle progression. In this review, we compile information on the primary response of plants in the regulation of the cell cycle in response to environmental stresses and show how the cell cycle proteins (mainly the cyclin-dependent kinases) involved in this regulation can act as components of environmental response signaling cascades, triggering adaptive responses to drive the cycle through climate fluctuations. Understanding the roles of CDKs and their regulators in the face of adversity may be crucial to meeting the challenge of increasing agricultural productivity in a new climate.

scholarly journals Genome-Wide Analysis of Cell Cycle-Regulating Genes in the Symbiotic Dinoflagellate Breviolum minutum

2019 ◽  
Vol 9 (11) ◽  
pp. 3843-3853 ◽  
Author(s):  
Michael L. Cato ◽  
Hallie D. Jester ◽  
Adam Lavertu ◽  
Audrey Lyman ◽  
Lacey M. Tallent ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Symbiotic Dinoflagellate ◽  
Genome Wide Analysis ◽  
Genome Wide

Bcr-Abl kinase down-regulates cyclin-dependent kinase inhibitor p27 in human and murine cell lines

Blood ◽  
2000 ◽  
Vol 96 (5) ◽  
pp. 1933-1939 ◽  
Author(s):  
Tarja Jonuleit ◽  
Heiko van der Kuip ◽  
Cornelius Miething ◽  
Heike Michels ◽  
Michael Hallek ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Kinase Inhibitor ◽  
Down Regulation ◽  
Cycle Progression ◽  
Cyclin Dependent Kinases ◽  
Abl Kinase

Abstract Chronic myeloid leukemia (CML) is a malignant stem cell disease characterized by an expansion of myeloid progenitor cells expressing the constitutively activated Bcr-Abl kinase. This oncogenic event causes a deregulation of apoptosis and cell cycle progression. Although the molecular mechanisms protecting from apoptosis in CML cells are well characterized, the cell cycle regulatory event is poorly understood. An inhibitor of the cyclin-dependent kinases, p27, plays a central role in the regulation of growth factor dependent proliferation of hematopoietic cells. Therefore, we have analyzed the influence of Bcr-Abl in the regulation of p27 expression in various hematopoietic cell systems. An active Bcr-Abl kinase causes down-regulation of p27 expression in murine Ba/F3 cells and human M07 cells. Bcr-Abl blocks up-regulation of p27 after growth factor withdrawal and serum reduction. In addition, p27 induction by transforming growth factor-beta (TGF-β) is completely blocked in Bcr-Abl positive M07/p210 cells. This deregulation is directly mediated by the activity of the Bcr-Abl kinase. A Bcr-Abl kinase inhibitor completely abolishes p27 down-regulation by Bcr-Abl in both Ba/F3 cells transfected either with a constitutively active Bcr-Abl or with a temperature sensitive mutant. The down-regulation of p27 by Bcr-Abl depends on proteasomal degradation and can be blocked by lactacystin. Overexpression of wild-type p27 partially antagonizes Bcr-Abl–induced proliferation in Ba/F3 cells. We conclude that Bcr-Abl promotes cell cycle progression and activation of cyclin-dependent kinases by interfering with the regulation of the cell cycle inhibitory protein p27.

scholarly journals Deacetylation of catalytic lysine in CDK1 is essential for Cyclin-B binding and cell cycle

2018 ◽  
Author(s):  
Shaunak Deota ◽  
Sivasudhan Rathnachalam ◽  
Kanojia Namrata ◽  
Mayank Boob ◽  
Amit Fulzele ◽  
...  
Keyword(s):  
Cell Cycle ◽  
High Resolution ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Current Model ◽  
Cyclin B ◽  
Cycle Progression ◽  
Cyclin Dependent Kinases ◽  
Evolutionarily Conserved ◽  
Cycle Dependent

AbstractCyclin-dependent-kinases (CDKs) are essential for cell cycle progression. While dependence of CDK activity on Cyclin levels is established, molecular mechanisms that regulate their binding are less studied. Here, we show that CDKl:Cyclin-B interactions are regulated by acetylation, which was hitherto unknown. We demonstrate that cell cycle dependent acetylation of the evolutionarily conserved catalytic lysine in CDK1 or eliminating its charge state abrogates Cyclin-B binding. Opposing activities of SIRT1 and P300 regulate acetylation, which marks a reserved pool of CDK1. Our high resolution structural analyses into the formation of kinase competent CDK1: Cyclin-B complex have unveiled long-range effects of catalytic lysine in configuring the CDK1 interface for Cyclin-B binding. Cells expressing acetylation mimic mutant of Cdc2 in yeast are arrested in G2 and fail to divide. Thus, by illustrating cell cycle dependent deacetylation as a determinant of CDK1:Cyclin-B interaction, our results redefine the current model of CDK1 activation and cell cycle progression.

Bcr-Abl kinase down-regulates cyclin-dependent kinase inhibitor p27 in human and murine cell lines

Blood ◽  
2000 ◽  
Vol 96 (5) ◽  
pp. 1933-1939 ◽  
Author(s):  
Tarja Jonuleit ◽  
Heiko van der Kuip ◽  
Cornelius Miething ◽  
Heike Michels ◽  
Michael Hallek ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Kinase Inhibitor ◽  
Down Regulation ◽  
Cycle Progression ◽  
Cyclin Dependent Kinases ◽  
Abl Kinase

Chronic myeloid leukemia (CML) is a malignant stem cell disease characterized by an expansion of myeloid progenitor cells expressing the constitutively activated Bcr-Abl kinase. This oncogenic event causes a deregulation of apoptosis and cell cycle progression. Although the molecular mechanisms protecting from apoptosis in CML cells are well characterized, the cell cycle regulatory event is poorly understood. An inhibitor of the cyclin-dependent kinases, p27, plays a central role in the regulation of growth factor dependent proliferation of hematopoietic cells. Therefore, we have analyzed the influence of Bcr-Abl in the regulation of p27 expression in various hematopoietic cell systems. An active Bcr-Abl kinase causes down-regulation of p27 expression in murine Ba/F3 cells and human M07 cells. Bcr-Abl blocks up-regulation of p27 after growth factor withdrawal and serum reduction. In addition, p27 induction by transforming growth factor-beta (TGF-β) is completely blocked in Bcr-Abl positive M07/p210 cells. This deregulation is directly mediated by the activity of the Bcr-Abl kinase. A Bcr-Abl kinase inhibitor completely abolishes p27 down-regulation by Bcr-Abl in both Ba/F3 cells transfected either with a constitutively active Bcr-Abl or with a temperature sensitive mutant. The down-regulation of p27 by Bcr-Abl depends on proteasomal degradation and can be blocked by lactacystin. Overexpression of wild-type p27 partially antagonizes Bcr-Abl–induced proliferation in Ba/F3 cells. We conclude that Bcr-Abl promotes cell cycle progression and activation of cyclin-dependent kinases by interfering with the regulation of the cell cycle inhibitory protein p27.

scholarly journals CpG Oligodeoxynucleotide Promotes Apoptosis of Human Bladder Cancer T24 Cells Via Inhibition of the Antiapoptotic Factors

2019 ◽  
Vol 18 ◽  
pp. 153303381987363 ◽  
Author(s):  
Yang Luo ◽  
Yuhang Dong ◽  
Shengran Liang ◽  
Lihong Yuan ◽  
Hongsheng Men ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Molecular Mechanisms ◽  
B Cell Lymphoma ◽  
Cell Cycle Phase ◽  
Bladder Cancer Cell Line ◽  
Cycle Phase ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
T24 Cells

Objective: Unmethylated cytosine-phosphorothioate-guanine oligodeoxynucleotide, a synthetic oligodeoxynucleotide, has been used as an adjuvant in clinic and in the antitumor activity. However, the antitumor mechanism of cytosine-phosphorothioate-guanine oligodeoxynucleotide against human bladder cancer is unknown. The purpose of this study is to evaluate the cytotoxicity and molecular mechanism of anticancer effect of cytosine-phosphorothioate-guanine oligodeoxynucleotide on T24 cells (a human bladder cancer cell line). Methods: The cytotoxic activity of cytosine-phosphorothioate-guanine oligodeoxynucleotide was examined by cell viability assay in the presence and absence of 5-fluorouracil, respectively. Apoptosis and cell-cycle phase distribution were detected by flow cytometry analysis. To investigate the molecular mechanisms of cytosine-phosphorothioate-guanine oligodeoxynucleotide cytotoxicity, the expression of antiapoptotic factors (B-cell lymphoma-2 and Survivin, β-actin as control) in RNA, and protein level was assayed by quantitative real-time polymerase chain reaction and automated capillary Western blot. Results: The inhibition ratio of T24 cells treated with both cytosine-phosphorothioate-guanine oligodeoxynucleotide and 5-fluorouracil was higher than those treated with either cytosine-phosphorothioate-guanine oligodeoxynucleotide or 5-fluorouracil alone. In the combination group (cytosine-phosphorothioate-guanine oligodeoxynucleotide and 5-fluorouracil), the apoptosis rate was significantly increased, and more cells were arrested at “S” and “G2/M” phases compared to those in cytosine-phosphorothioate-guanine oligodeoxynucleotide or 5-fluorouracil alone. Furthermore, the expression of antiapoptotic factors was decreased by cytosine-phosphorothioate-guanine oligodeoxynucleotide alone or combined with 5-fluorouracil. Conclusion: Cytosine-phosphorothioate-guanine oligodeoxynucleotide promoted apoptosis and enhanced the chemosensitivity of 5-fluorouracil in T24 cells. Cytosine-phosphorothioate-guanine oligodeoxynucleotide downregulated the expression of antiapoptotic factors and inhibited cell-cycle phase by arresting more cells at “S” and “G2/M” phases. This study indicated the potential ability of cytosine-phosphorothioate-guanine oligodeoxynucleotide as a candidate drug for human bladder cancer.

scholarly journals Involvement of the Cell Wall Integrity Pathway of Saccharomyces cerevisiae in Protection against Cadmium and Arsenate Stresses

2020 ◽  
Vol 86 (21) ◽  
Author(s):  
Todsapol Techo ◽  
Sirada Charoenpuntaweesin ◽  
Choowong Auesukaree
Keyword(s):  
Cell Cycle ◽  
Cell Wall ◽  
Molecular Mechanisms ◽  
Cell Cycle Control ◽  
Protective Role ◽  
Cell Wall Integrity ◽  
Cycle Phase ◽  
Cell Wall Biosynthesis ◽  
Cell Wall Modification ◽  
Content Type

ABSTRACT Contamination of soil and water with heavy metals and metalloids is a serious environmental problem. Cadmium and arsenic are major environmental contaminants that pose a serious threat to human health. Although toxicities of cadmium and arsenic to living organisms have been extensively studied, the molecular mechanisms of cellular responses to cadmium and arsenic remain poorly understood. In this study, we demonstrate that the cell wall integrity (CWI) pathway is involved in coping with cell wall stresses induced by cadmium and arsenate through its role in the regulation of cell wall modification. Interestingly, the Rlm1p and SBF (Swi4p-Swi6p) complex transcription factors of the CWI pathway were shown to be specifically required for tolerance to cadmium and arsenate, respectively. Furthermore, we found the PIR2 gene, encoding cell wall O-mannosylated heat shock protein, whose expression is under the control of the CWI pathway, is important for maintaining cell wall integrity during cadmium and arsenate stresses. In addition, our results revealed that the CWI pathway is involved in modulating the expression of genes involved in cell wall biosynthesis and cell cycle control in response to cadmium and arsenate via distinct sets of transcriptional regulators. IMPORTANCE Environmental pollution by metal/metalloids such as cadmium and arsenic has become a serious problem in many countries, especially in developing countries. This study shows that in the yeast S. cerevisiae, the CWI pathway plays a protective role against cadmium and arsenate through the upregulation of genes involved in cell wall biosynthesis and cell cycle control, possibly in order to modulate cell wall reconstruction and cell cycle phase transition, respectively. These data provide insights into molecular mechanisms underlying adaptive responses to cadmium and arsenate.

scholarly journals DEAD-Box RNA Helicases in Cell Cycle Control and Clinical Therapy

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1540
Author(s):  
Lu Zhang ◽  
Xiaogang Li
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Direct Interaction ◽  
Large Family ◽  
Cycle Phase ◽  
Rna Helicases ◽  
Diverse Range ◽  
Ribonucleoprotein Complexes

Cell cycle is regulated through numerous signaling pathways that determine whether cells will proliferate, remain quiescent, arrest, or undergo apoptosis. Abnormal cell cycle regulation has been linked to many diseases. Thus, there is an urgent need to understand the diverse molecular mechanisms of how the cell cycle is controlled. RNA helicases constitute a large family of proteins with functions in all aspects of RNA metabolism, including unwinding or annealing of RNA molecules to regulate pre-mRNA, rRNA and miRNA processing, clamping protein complexes on RNA, or remodeling ribonucleoprotein complexes, to regulate gene expression. RNA helicases also regulate the activity of specific proteins through direct interaction. Abnormal expression of RNA helicases has been associated with different diseases, including cancer, neurological disorders, aging, and autosomal dominant polycystic kidney disease (ADPKD) via regulation of a diverse range of cellular processes such as cell proliferation, cell cycle arrest, and apoptosis. Recent studies showed that RNA helicases participate in the regulation of the cell cycle progression at each cell cycle phase, including G1-S transition, S phase, G2-M transition, mitosis, and cytokinesis. In this review, we discuss the essential roles and mechanisms of RNA helicases in the regulation of the cell cycle at different phases. For that, RNA helicases provide a rich source of targets for the development of therapeutic or prophylactic drugs. We also discuss the different targeting strategies against RNA helicases, the different types of compounds explored, the proposed inhibitory mechanisms of the compounds on specific RNA helicases, and the therapeutic potential of these compounds in the treatment of various disorders.

scholarly journals O-3 The cell cycle phase influences the accuracy of single cell genome wide array-CGH

2013 ◽  
Vol 26 ◽  
pp. S14
Author(s):  
E. Dimitriadou ◽  
N. Van der Aa ◽  
S. Ardui ◽  
J. Cheng ◽  
Y. Moreau ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Single Cell ◽  
Array Cgh ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Genome Wide ◽  
Cell Genome ◽  
Single Cell Genome
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