scholarly journals Glucose Regulation of Saccharomyces cerevisiae Cell Cycle Genes

2003 ◽  
Vol 2 (1) ◽  
pp. 143-149 ◽  
Author(s):  
Laura L. Newcomb ◽  
Jasper A. Diderich ◽  
Matthew G. Slattery ◽  
Warren Heideman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Glucose Repression ◽  
Nutrient Sensing ◽  
Glucose Response ◽  
Glucose Signaling ◽  
Expression Of Genes ◽  
Proliferative Growth ◽  
Cell Cycle Regulatory Proteins ◽  
Glucose Induction

ABSTRACT Nutrient-limited Saccharomyces cerevisiae cells rapidly resume proliferative growth when transferred into glucose medium. This is preceded by a rapid increase in CLN3, BCK2, and CDC28 mRNAs encoding cell cycle regulatory proteins that promote progress through Start. We have tested the ability of mutations in known glucose signaling pathways to block glucose induction of CLN3, BCK2, and CDC28. We find that loss of the Snf3 and Rgt2 glucose sensors does not block glucose induction, nor does deletion of HXK2, encoding the hexokinase isoenzyme involved in glucose repression signaling. Rapamycin blockade of the Tor nutrient sensing pathway does not block the glucose response. Addition of 2-deoxy glucose to the medium will not substitute for glucose. These results indicate that glucose metabolism generates the signal required for induction of CLN3, BCK2, and CDC28. In support of this conclusion, we find that addition of iodoacetate, an inhibitor of the glyceraldehyde-3-phosphate dehydrogenase step in yeast glycolysis, strongly downregulates the levels CLN3, BCK2, and CDC28 mRNAs. Furthermore, mutations in PFK1 and PFK2, which encode phosphofructokinase isoforms, inhibit glucose induction of CLN3, BCK2, and CDC28. These results indicate a link between the rate of glycolysis and the expression of genes that are critical for passage through G1.

scholarly journals Regulatory Network Connecting Two Glucose Signal Transduction Pathways in Saccharomyces cerevisiae

2004 ◽  
Vol 3 (1) ◽  
pp. 221-231 ◽  
Author(s):  
Aneta Kaniak ◽  
Zhixiong Xue ◽  
Daniel Macool ◽  
Jeong-Ho Kim ◽  
Mark Johnston
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Signal Transduction ◽  
Transcription Factor ◽  
Regulatory Network ◽  
Target Genes ◽  
Glucose Repression ◽  
Signal Transduction Pathways ◽  
Glucose Signaling ◽  
Genes Encoding ◽  
Glucose Induction

ABSTRACT The yeast Saccharomyces cerevisiae senses glucose, its preferred carbon source, through multiple signal transduction pathways. In one pathway, glucose represses the expression of many genes through the Mig1 transcriptional repressor, which is regulated by the Snf1 protein kinase. In another pathway, glucose induces the expression of HXT genes encoding glucose transporters through two glucose sensors on the cell surface that generate an intracellular signal that affects function of the Rgt1 transcription factor. We profiled the yeast transcriptome to determine the range of genes targeted by this second pathway. Candidate target genes were verified by testing for Rgt1 binding to their promoters by chromatin immunoprecipitation and by measuring the regulation of the expression of promoter lacZ fusions. Relatively few genes could be validated as targets of this pathway, suggesting that this pathway is primarily dedicated to regulating the expression of HXT genes. Among the genes regulated by this glucose signaling pathway are several genes involved in the glucose induction and glucose repression pathways. The Snf3/Rgt2-Rgt1 glucose induction pathway contributes to glucose repression by inducing the transcription of MIG2, which encodes a repressor of glucose-repressed genes, and regulates itself by inducing the expression of STD1, which encodes a regulator of the Rgt1 transcription factor. The Snf1-Mig1 glucose repression pathway contributes to glucose induction by repressing the expression of SNF3 and MTH1, which encodes another regulator of Rgt1, and also regulates itself by repressing the transcription of MIG1. Thus, these two glucose signaling pathways are intertwined in a regulatory network that serves to integrate the different glucose signals operating in these two pathways.

scholarly journals Integration of Transcriptional and Posttranslational Regulation in a Glucose Signal Transduction Pathway in Saccharomyces cerevisiae

2006 ◽  
Vol 5 (1) ◽  
pp. 167-173 ◽  
Author(s):  
Jeong-Ho Kim ◽  
Valérie Brachet ◽  
Hisao Moriya ◽  
Mark Johnston
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Glucose Repression ◽  
Signal Transduction Pathway ◽  
Feedback Regulation ◽  
Glucose Sensing ◽  
26S Proteasome ◽  
Posttranslational Regulation ◽  
Glucose Signaling ◽  
Genes Encoding ◽  
Glucose Induction

ABSTRACT Expression of the HXT genes encoding glucose transporters in the budding yeast Saccharomyces cerevisiae is regulated by two interconnected glucose-signaling pathways: the Snf3/Rgt2-Rgt1 glucose induction pathway and the Snf1-Mig1 glucose repression pathway. The Snf3 and Rgt2 glucose sensors in the membrane generate a signal in the presence of glucose that inhibits the functions of Std1 and Mth1, paralogous proteins that regulate the function of the Rgt1 transcription factor, which binds to the HXT promoters. It is well established that glucose induces degradation of Mth1, but the fate of its paralogue Std1 has been less clear. We present evidence that glucose-induced degradation of Std1 via the SCFGrr1 ubiquitin-protein ligase and the 26S proteasome is obscured by feedback regulation of STD1 expression. Disappearance of Std1 in response to glucose is accelerated when glucose induction of STD1 expression due to feedback regulation by Rgt1 is prevented. The consequence of relieving feedback regulation of STD1 expression is that reestablishment of repression of HXT1 expression upon removal of glucose is delayed. In contrast, degradation of Mth1 is reinforced by glucose repression of MTH1 expression: disappearance of Mth1 is slowed when glucose repression of MTH1 expression is prevented, and this results in a delay in induction of HXT3 expression in response to glucose. Thus, the cellular levels of Std1 and Mth1, and, as a consequence, the kinetics of induction and repression of HXT gene expression, are closely regulated by interwoven transcriptional and posttranslational controls mediated by two different glucose-sensing pathways.

scholarly journals Glucose Signaling-Mediated Coordination of Cell Growth and Cell Cycle in Saccharomyces Cerevisiae

Sensors ◽  
2010 ◽  
Vol 10 (6) ◽  
pp. 6195-6240 ◽  
Author(s):  
Stefano Busti ◽  
Paola Coccetti ◽  
Lilia Alberghina ◽  
Marco Vanoni
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Growth ◽  
Glucose Signaling

scholarly journals Transcriptional Analysis of the Candida albicans Cell Cycle

2009 ◽  
Vol 20 (14) ◽  
pp. 3363-3373 ◽  
Author(s):  
Pierre Côte ◽  
Hervé Hogues ◽  
Malcolm Whiteway
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Candida Albicans ◽  
Pathogenic Fungus ◽  
Transcriptional Analysis ◽  
Pathogenic Yeast ◽  
Homologous Genes ◽  
Regulatory Circuit ◽  
Expression Of Genes ◽  
Human Pathogenic Fungus

We have examined the periodic expression of genes through the cell cycle in cultures of the human pathogenic fungus Candida albicans synchronized by mating pheromone treatment. Close to 500 genes show increased expression during the G1, S, G2, or M transitions of the C. albicans cell cycle. Comparisons of these C. albicans periodic genes with those already found in the budding and fission yeasts and in human cells reveal that of 2200 groups of homologous genes, close to 600 show periodicity in at least one organism, but only 11 are periodic in all four species. Overall, the C. albicans regulatory circuit most closely resembles that of Saccharomyces cerevisiae but contains a simplified structure. Although the majority of the C. albicans periodically regulated genes have homologues in the budding yeast, 20% (100 genes), most of which peak during the G1/S or M/G1 transitions, are unique to the pathogenic yeast.

scholarly journals Snf1 Kinase Connects Nutritional Pathways Controlling Meiosis in Saccharomyces cerevisiae

1998 ◽  
Vol 18 (8) ◽  
pp. 4548-4555 ◽  
Author(s):  
Saul M. Honigberg ◽  
Rita H. Lee
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Glucose Repression ◽  
Acetate Metabolism ◽  
Sporulation Medium ◽  
Multicopy Plasmid ◽  
Snf1 Kinase ◽  
Expression Of Genes ◽  
Regulatory Effects ◽  
Meiotic Initiation

ABSTRACT Glucose inhibits meiosis in Saccharomyces cerevisiae at three different steps (IME1 transcription, IME2transcription, and entry into late stages of meiosis). Because many of the regulatory effects of glucose in yeast are mediated through the inhibition of Snf1 kinase, a component of the glucose repression pathway, we determined the role of SNF1 in regulating meiosis. Deleting SNF1 repressed meiosis at the same three steps that were inhibited by glucose, suggesting that glucose blocks meiosis by inhibiting Snf1. For example, the snf1Δ mutant completely failed to induce IME1 transcripts in sporulation medium. Furthermore, even when this block was bypassed by expression ofIME1 from a multicopy plasmid, IME2transcription and meiotic initiation occurred at only 10 to 20% of the levels seen in wild-type cells. The addition of glucose did not further inhibit IME2 transcription, suggesting that Snf1 is the primary mediator of glucose controls on IME2 expression. Finally, in snf1Δ cells in which both blocks on meiotic initiation were bypassed, early stages of meiosis (DNA replication and commitment to recombination) occurred, but later stages (chromosome segregation and spore formation) did not, suggesting that Snf1 controls later stages of meiosis independently from the two controls on meiotic initiation. Because Snf1 is known to activate the expression of genes required for acetate metabolism, it may also serve to connect glucose and acetate controls on meiotic differentiation.

Mutations in GSF1 and GSF2 Alter Glucose Signaling in Saccharomyces cerevisiae

Genetics ◽  
1997 ◽  
Vol 147 (2) ◽  
pp. 557-566 ◽  
Author(s):  
Peter W Sherwood ◽  
Marian Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Slow Growth ◽  
Glucose Repression ◽  
Snf1 Kinase ◽  
Glucose Signaling ◽  
Glucose Depletion ◽  
Complementation Groups ◽  
Growth Phenotype ◽  
His3 Gene ◽  
Slow Growth Phenotype

One function of the Saccharomyces cerevisiae Snf1 protein kinase is to relieve glucose repression of SUC, GAL, and other genes in response to glucose depletion. To identify genes that regulate Snf1 kinase activity, we have selected mutants that inappropriately express a SUC2promoter::HIS3 gene fusion when grown in glucose and that require Snf1 function for this phenotype. Mutations representing two new complementation groups (gsf1 and gsf2) were isolated. gsf1 mutations affect two distinct responses to glucose: the Snf1-regulated glucose repression of SUC2 and GAL10 transcription and the Snf1-independent induction by glucose of HXT1 transcription. gsf2 mutations relieve glucose repression of SUC2 and GAL10 transcription and, in combination with snf1Δ, cause an extreme slow growth phenotype. The GSF2 gene was cloned by complementation of the gsf2-1 snf1Δ slow growth phenotype and encodes a previously uncharacterized 46 kD protein.

The Role of Retinoblastoma Protein in Cell Cycle Regulation: An Updated Review

2021 ◽  
Vol 20 ◽  
Author(s):  
Rabih Roufayel ◽  
Rabih Mezher ◽  
Kenneth B. Storey
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Transcription Factors ◽  
Cell Cycle Control ◽  
Expression Of Genes ◽  
E2f Transcription Factor ◽  
Cellular Energetics ◽  
Development And Differentiation ◽  
E2f Transcription Factors ◽  
Rb Phosphorylation

: Selected transcription factors have critical roles to play in organism survival by regulating the expression of genes that control the adaptations needed to handle stress conditions. The retinoblastoma (Rb) protein coupled with the E2F transcription factor family was demonstrated to have roles in controlling the cell cycle during freezing and associated environmental stresses (anoxia, dehydration). Rb phosphorylation or acetylation at different sites provide a mechanism for repressing cell proliferation that is under the control of E2F transcription factors in animals facing stresses that disrupt cellular energetics or cell volume controls. Other central regulators of the cell cycle including Cyclins, Cyclin dependent kinases (Cdks), and checkpoint proteins detect DNA damage or any improper replication, blocking further progression of cell cycle and interrupting cell proliferation. This review provides an insight into the molecular regulatory mechanisms of cell cycle control, focusing on Rb-E2F along with Cyclin-Cdk complexes typically involved in development and differentiation that need to be regulated in order to survive extreme cellular stress.

scholarly journals Effects of Aspergillus fumigatus Conidia on Apoptosis and Proliferation in an In Vitro Model of the Lung Microenvironment

2021 ◽  
Vol 9 (7) ◽  
pp. 1435
Author(s):  
Hisako Kushima ◽  
Toshiyuki Tsunoda ◽  
Taichi Matsumoto ◽  
Yoshiaki Kinoshita ◽  
Koichi Izumikawa ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Epithelial Cells ◽  
Pulmonary Fibrosis ◽  
Aspergillus Fumigatus ◽  
Rna Sequencing ◽  
A549 Cells ◽  
Western Blots ◽  
Mesenchymal Transition ◽  
Expression Of Genes ◽  
Nih 3T3

Background/Aim: Aspergillus is often detected in respiratory samples from patients with chronic respiratory diseases, including pulmonary fibrosis, suggesting that it can easily colonize the airways. To determine the role of Aspergillus colonization in pulmonary fibrosis, we cultured human lung epithelial A549 cells or murine embryo fibroblast NIH/3T3 cells with Aspergillus conidia in 3D floating culture representing the microenvironment. Materials and Methods: Cells were cultured in two-dimensional (2D) and three-dimensional floating (3DF) culture with heat-inactivated Aspergillus fumigatus (AF) 293 conidia at an effector-to-target cell ratio of 1:10 (early-phase model) and 1:100 (colonization model), and RNA-sequencing and Western blots (WB) were performed. Results: AF293 conidia reduced A549 cell growth in 2D and 3DF cultures and induced apoptosis in A549 spheroids in 3DF culture. RNA-sequencing revealed the increased expression of genes associated with interferon-mediated antiviral responses including MX dymamin-like GTPase 1 (MX1). Interestingly, the decreased expression of genes associated with the cell cycle was observed with a high concentration of AF293 conidia. WB revealed that epithelial-mesenchymal transition was not involved. Notably, AF293 conidia increased NIH/3T3 growth only in 3DF culture without inducing an apoptotic reaction. RNA-sequencing revealed the increased expression of genes associated with interferon signalling, including MX2; however, the decreased expression of genes associated with the cell cycle was not observed. Conclusions: AF affects both apoptosis of epithelial cells and the growth of fibroblasts. A deeper understanding of the detailed mechanisms underlying Aspergillus-mediated signaling pathway in epithelial cells and fibroblasts will help us to understand the lung microenvironment.

Yeast dom34 Mutants Are Defective in Multiple Developmental Pathways and Exhibit Decreased Levels of Polyribosomes

Genetics ◽  
1998 ◽  
Vol 149 (1) ◽  
pp. 45-56
Author(s):  
Luther Davis ◽  
JoAnne Engebrecht
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Heterologous Expression ◽  
Protein Translation ◽  
Developmental Pathways ◽  
G1 Phase ◽  
Growth Defect ◽  
Wild Type ◽  
Drosophila Homolog ◽  
Mutant Cells

Abstract The DOM34 gene of Saccharomyces cerevisiae is similar togenes found in diverse eukaryotes and archaebacteria. Analysis of dom34 strains shows that progression through the G1 phase of the cell cycle is delayed, mutant cells enter meiosis aberrantly, and their ability to form pseudohyphae is significantly diminished. RPS30A, which encodes ribosomal protein S30, was identified in a screen for high-copy suppressors of the dom34Δ growth defect. dom34Δ mutants display an altered polyribosome profile that is rescued by expression of RPS30A. Taken together, these data indicate that Dom34p functions in protein translation to promote G1 progression and differentiation. A Drosophila homolog of Dom34p, pelota, is required for the proper coordination of meiosis and spermatogenesis. Heterologous expression of pelota in dom34Δ mutants restores wild-type growth and differentiation, suggesting conservation of function between the eukaryotic members of the gene family.

scholarly journals Recombination of Ty elements in yeast can be induced by a double-strand break.

Genetics ◽  
1995 ◽  
Vol 140 (1) ◽  
pp. 67-77 ◽  
Author(s):  
A Parket ◽  
O Inbar ◽  
M Kupiec
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Strand Break ◽  
Double Strand Break ◽  
The Other ◽  
Direct Repeats ◽  
Yeast Saccharomyces Cerevisiae ◽  
Low Frequencies ◽  
Ty Elements ◽  
Main Family

Abstract The Ty retrotransposons are the main family of dispersed repeated sequences in the yeast Saccharomyces cerevisiae. These elements are flanked by a pair of long terminal direct repeats (LTRs). Previous experiments have shown that Ty elements recombine at low frequencies, despite the fact that they are present in 30 copies per genome. This frequency is not highly increased by treatments that cause DNA damage, such as UV irradiation. In this study, we show that it is possible to increase the recombination level of a genetically marked Ty by creating a double-strand break in it. This break is repaired by two competing mechanisms: one of them leaves a single LTR in place of the Ty, and the other is a gene conversion event in which the marked Ty is replaced by an ectopically located one. In a strain in which the marked Ty has only one LTR, the double-strand break is repaired by conversion. We have also measured the efficiency of repair and monitored the progression of the cells through the cell-cycle. We found that in the presence of a double-strand break in the marked Ty, a proportion of the cells is unable to resume growth.

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