scholarly journals CLN1 and Its Repression by Xbp1 Are Important for Efficient Sporulation in Budding Yeast

2000 ◽  
Vol 20 (2) ◽  
pp. 478-487 ◽  
Author(s):  
Bernard Mai ◽  
Linda Breeden
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Differential Display ◽  
Mitotic Cycle ◽  
Target Genes ◽  
Budding Yeast ◽  
Transcriptional Repressor ◽  
Primary Target ◽  
New Class ◽  
Genes Encoding ◽  
Meiotic Cycle

ABSTRACT Xbp1, a transcriptional repressor of Saccharomyces cerevisiae with homology to Swi4 and Mbp1, is induced by stress and starvation during the mitotic cycle. It is also induced late in the meiotic cycle. Using RNA differential display, we find that genes encoding three cyclins (CLN1, CLN3, andCLB2), CYS3, and SMF2 are downregulated when Xbp1 is overexpressed and that Xbp1 can bind to sequences in their promoters. During meiosis, XBP1 is highly induced and its mRNA appears at the same time asDIT1 mRNA, but its expression remains high for up to 24 h. As such, it represents a new class of meiosis-specific genes. Xbp1-deficient cells are capable of forming viable gametes, although ascus formation is delayed by several hours. Furthermore, Xbp1 target genes are normally repressed late in meiosis, and loss ofXBP1 results in their derepression. Interestingly, we find that a deletion of CLN1 also reduces the efficiency of sporulation and delays the meiotic program but that sporulation in a Δcln1 Δxbp1 strain is not further delayed. Thus, CLN1 may be Xbp1's primary target in meiotic cells. We hypothesize that CLN1 plays a role early in the meiotic program but must be repressed, by Xbp1, at later stages to promote efficient sporulation.

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 Grr1-dependent Inactivation of Mth1 Mediates Glucose-induced Dissociation of Rgt1 from HXT Gene Promoters

2003 ◽  
Vol 14 (8) ◽  
pp. 3230-3241 ◽  
Author(s):  
Karin M. Flick ◽  
Nathalie Spielewoy ◽  
Tatyana I. Kalashnikova ◽  
Marisela Guaderrama ◽  
Qianzheng Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Budding Yeast ◽  
Transcriptional Repressor ◽  
Gene Promoters ◽  
Negative Regulators ◽  
Dependent Inactivation ◽  
Genes Encoding ◽  
F Box Protein

In budding yeast, HXT genes encoding hexose permeases are induced by glucose via a mechanism in which the F box protein Grr1 antagonizes activity of the transcriptional repressor Rgt1. Neither the mechanism of Rgt1 inactivation nor the role of Grr1 in that process has been understood. We show that glucose promotes phosphorylation of Rgt1 and its dissociation from HXT gene promoters. This cascade of events is dependent upon the F-box protein Grr1. Inactivation of Rgt1 is sufficient to explain the requirement for Grr1 but does not involve Rgt1 proteolysis or ubiquitination. We show that inactivation of Mth1 and Std1, known negative regulators of HXT gene expression, leads to the hyperphosphorylation of Rgt1 and its dissociation from HXT promoters even in the absence of glucose. Furthermore, inactivation of Mth1 and Std1 bypasses the requirement for Grr1 for induction of these events, suggesting they are targets for inactivation by Grr1. Consistent with that proposal, Mth1 is rapidly eliminated in response to glucose via a mechanism that requires Grr1. Based upon these data, we propose that glucose acts via Grr1 to promote the degradation of Mth1. Degradation of Mth1 leads to phosphorylation and dissociation of Rgt1 from HXT promoters, thereby activating HXT gene expression.

Transcriptional Repressor Rdr1 Negatively Regulates Stress Response in Budding Yeast Saccharomyces cerevisiae*

2010 ◽  
Vol 2009 (12) ◽  
pp. 1544-1552
Author(s):  
Min MIAO ◽  
Hong-Ping CAO ◽  
Yan ZHONG ◽  
Jun LIU ◽  
Yi-Hui WANG ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Stress Response ◽  
Budding Yeast ◽  
Transcriptional Repressor

scholarly journals Adjustment of Trehalose Metabolism in Wine Saccharomyces cerevisiae Strains To Modify Ethanol Yields

2013 ◽  
Vol 79 (17) ◽  
pp. 5197-5207 ◽  
Author(s):  
D. Rossouw ◽  
E. H. Heyns ◽  
M. E. Setati ◽  
S. Bosch ◽  
F. F. Bauer
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Genetic Modification ◽  
Target Genes ◽  
Tca Cycle ◽  
Pentose Phosphate ◽  
Systematic Screening ◽  
Content Type ◽  
Genes Encoding ◽  
Ethanol Yields ◽  
Trehalose Biosynthesis

ABSTRACTThe ability ofSaccharomyces cerevisiaeto efficiently produce high levels of ethanol through glycolysis has been the focus of much scientific and industrial activity. Despite the accumulated knowledge regarding glycolysis, the modification of flux through this pathway to modify ethanol yields has proved difficult. Here, we report on the systematic screening of 66 strains with deletion mutations of genes encoding enzymes involved in central carbohydrate metabolism for altered ethanol yields. Five of these strains showing the most prominent changes in carbon flux were selected for further investigation. The genes were representative of trehalose biosynthesis (TPS1, encoding trehalose-6-phosphate synthase), central glycolysis (TDH3, encoding glyceraldehyde-3-phosphate dehydrogenase), the oxidative pentose phosphate pathway (ZWF1, encoding glucose-6-phosphate dehydrogenase), and the tricarboxylic acid (TCA) cycle (ACO1andACO2, encoding aconitase isoforms 1 and 2). Two strains exhibited lower ethanol yields than the wild type (tps1Δ andtdh3Δ), while the remaining three showed higher ethanol yields. To validate these findings in an industrial yeast strain, theTPS1gene was selected as a good candidate for genetic modification to alter flux to ethanol during alcoholic fermentation in wine. Using low-strength promoters active at different stages of fermentation, the expression of theTPS1gene was slightly upregulated, resulting in a decrease in ethanol production and an increase in trehalose biosynthesis during fermentation. Thus, the mutant screening approach was successful in terms of identifying target genes for genetic modification in commercial yeast strains with the aim of producing lower-ethanol wines.

scholarly journals Effects of overexpression of STB5 in Saccharomyces cerevisiae on fatty acid biosynthesis, physiology and transcriptome

2019 ◽  
Vol 19 (3) ◽  
Author(s):  
Alexandra Bergman ◽  
Dóra Vitay ◽  
John Hellgren ◽  
Yun Chen ◽  
Jens Nielsen ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Fatty Acid ◽  
Target Genes ◽  
Fatty Acid Biosynthesis ◽  
Pentose Phosphate ◽  
Attractive Alternative ◽  
Microbial Conversion ◽  
Glucose Limitation ◽  
Production Route ◽  
Genes Encoding

ABSTRACTMicrobial conversion of biomass to fatty acids (FA) and products derived thereof is an attractive alternative to the traditional oleochemical production route from animal and plant lipids. This study examined if NADPH-costly FA biosynthesis could be enhanced by overexpressing the transcription factor Stb5 in Saccharomyces cerevisiae. Stb5 activates expression of multiple genes encoding enzymes within the pentose phosphate pathway (PPP) and other NADPH-producing reactions. Overexpression of STB5 led to a decreased growth rate and an increased free fatty acid (FFA) production during growth on glucose. The improved FFA synthetic ability in the glucose phase was shown to be independent of flux through the oxidative PPP. RNAseq analysis revealed that STB5 overexpression had wide-ranging effects on the transcriptome in the batch phase, and appeared to cause a counterintuitive phenotype with reduced flux through the oxidative PPP. During glucose limitation, when an increased NADPH supply is likely less harmful, an overall induction of the proposed target genes of Stb5 (eg. GND1/2, TAL1, ALD6, YEF1) was observed. Taken together, the strategy of utilizing STB5 overexpression to increase NADPH supply for reductive biosynthesis is suggested to have potential in strains engineered to have strong ability to consume excess NADPH, alleviating a potential redox imbalance.

Gal3p and Gal1p interact with the transcriptional repressor Gal80p to form a complex of 1:1 stoichiometry

2002 ◽  
Vol 363 (3) ◽  
pp. 515-520 ◽  
Author(s):  
David J. TIMSON ◽  
Helen C. ROSS ◽  
Richard J. REECE
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Amino Acid ◽  
Gel Filtration ◽  
Transcriptional Repressor ◽  
Galactose Metabolism ◽  
Genetic Switch ◽  
Sequence Identity ◽  
Genes Encoding ◽  
Small Molecule Ligands ◽  
High Degree

The genes encoding the enzymes required for galactose metabolism in Saccharomyces cerevisiae are controlled at the level of transcription by a genetic switch consisting of three proteins: a transcriptional activator, Gal4p; a transcriptional repressor, Gal80p; and a ligand sensor, Gal3p. The switch is turned on in the presence of two small molecule ligands, galactose and ATP. Gal3p shows a high degree of sequence identity with Gal1p, the yeast galactokinase. We have mapped the interaction between Gal80p and Gal3p, which only occurs in the presence of both ligands, using protease protection experiments and have shown that this involves amino acid residue 331 of Gal80p. Gel-filtration experiments indicate that Gal3p, or the galactokinase Gal1p, interact directly with Gal80p to form a complex with 1:1 stoichiometry.

scholarly journals Functional Analysis of the PUT3 Transcriptional Activator of the Proline Utilization Pathway in Saccharomyces cerevisiae

Genetics ◽  
1996 ◽  
Vol 142 (4) ◽  
pp. 1069-1082
Author(s):  
Shelley Ann G des Etages ◽  
Darlene A Fahey ◽  
Richard J Reece ◽  
Marjorie C Brandriss
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Target Genes ◽  
Yeast Saccharomyces Cerevisiae ◽  
Central Domain ◽  
Mutant Proteins ◽  
Molecular Tests ◽  
Defective Mutant ◽  
Proline Utilization ◽  
Genes Encoding ◽  
Utilization Pathway

Abstract Proline can serve as a nitrogen source for the yeast Saccharomyces cerevisiae when preferred sources of nitrogen are absent from the growth medium. PUT3, the activator of the proline utilization pathway, is required for the transcription of the genes encoding the enzymes that convert proline to glutamate. PUT3 is a 979 amino acid protein that constitutively binds a short DNA sequence in the promoters of its target genes, but does not activate their expression in the absence of induction by proline and in the presence of preferred sources of nitrogen. To understand how PUT3 is converted from an inactive to an active state, a dissection of its functional domains has been undertaken. Biochemical and molecular tests, domain swapping experiments, and an analysis of activator-constitutive and activator-defective mutant proteins indicate that PUT3 is dimeric and activates transcription with its negatively charged carboxyterminus, which does not appear to contain a proline-responsive domain. A mutation in the conserved central domain found in many fungal activators interferes with activation without affecting DNA binding or protein stability. Intragenic suppressors of the central domain mutation have been isolated and analyzed.

scholarly journals Membrane-active Compounds Activate the Transcription Factors Pdr1 and Pdr3 Connecting Pleiotropic Drug Resistance and Membrane Lipid Homeostasis in Saccharomyces cerevisiae

2007 ◽  
Vol 18 (12) ◽  
pp. 4932-4944 ◽  
Author(s):  
Christoph Schüller ◽  
Yasmine M. Mamnun ◽  
Hubert Wolfger ◽  
Nathan Rockwell ◽  
Jeremy Thorner ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Drug Resistance ◽  
Transcription Factors ◽  
Target Genes ◽  
Membrane Lipid ◽  
Yeast Cells ◽  
Dependent Manner ◽  
Pleiotropic Drug Resistance ◽  
Zinc Cluster ◽  
Genes Encoding

The Saccharomyces cerevisiae zinc cluster transcription factors Pdr1 and Pdr3 mediate general drug resistance to many cytotoxic substances also known as pleiotropic drug resistance (PDR). The regulatory mechanisms that activate Pdr1 and Pdr3 in response to the various xenobiotics are poorly understood. In this study, we report that exposure of yeast cells to 2,4-dichlorophenol (DCP), benzyl alcohol, nonionic detergents, and lysophospholipids causes rapid activation of Pdr1 and Pdr3. Furthermore, Pdr1/Pdr3 target genes encoding the ATP-binding cassette proteins Pdr5 and Pdr15 confer resistance against these compounds. Genome-wide transcript analysis of wild-type and pdr1Δ pdr3Δ cells treated with DCP reveals most prominently the activation of the PDR response but also other stress response pathways. Polyoxyethylene-9-laurylether treatment produced a similar profile with regard to activation of Pdr1 and Pdr3, suggesting activation of these by detergents. The Pdr1/Pdr3 response element is sufficient to confer regulation to a reporter gene by these substances in a Pdr1/Pdr3-dependent manner. Our data indicate that compounds with potential membrane-damaging or -perturbing effects might function as an activating signal for Pdr1 and Pdr3, and they suggest a role for their target genes in membrane lipid organization or remodeling.

scholarly journals Differential Regulation of Ceramide Synthase Components LAC1 and LAG1 in Saccharomyces cerevisiae

2004 ◽  
Vol 3 (4) ◽  
pp. 880-892 ◽  
Author(s):  
Marcin Kolaczkowski ◽  
Anna Kolaczkowska ◽  
Barbara Gaigg ◽  
Roger Schneiter ◽  
W. Scott Moye-Rowley
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Target Genes ◽  
Growth Defect ◽  
Ceramide Synthase ◽  
Zinc Cluster ◽  
Coordinate Control ◽  
Genes Encoding ◽  
Regulatory Input ◽  
Sphingolipid Biosynthesis ◽  
Ceramide Production

ABSTRACT In Saccharomyces cerevisiae, the essential ceramide synthase reaction requires the presence of one of a homologous pair of genes, LAG1 and LAC1. Mutants that lack both of these genes cannot produce ceramide and exhibit a striking synthetic growth defect. While the regulation of ceramide production is critical for the control of proliferation and for stress tolerance, little is known of the mechanisms that ensure proper control of this process. The data presented here demonstrate that the pleiotropic drug resistance (Pdr) regulatory pathway regulates the transcription of multiple genes encoding steps in sphingolipid biosynthesis, including LAC1. The zinc cluster transcriptional activators Pdr1p and Pdr3p bind to Pdr1p/Pdr3p-responsive elements (PDREs) in the promoters of Pdr pathway target genes. LAC1 contains a single PDRE in its promoter, but notably, LAG1 does not. Reporter gene, Northern blot, and Western blot assays indicated that the expression level of Lac1p is approximately three times that of Lag1p. Detailed analyses of the LAC1 promoter demonstrated that transcription of this gene is inhibited by the presence of the transcription factor Cbf1p and the anaerobic repressor Rox1p. LAG1 transcription was also elevated in cbf1Δ cells, indicating at least one common regulatory input. Although a hyperactive Pdr pathway altered the profile of sphingolipids produced, the loss of either LAC1 or LAG1 alone failed to produce further changes. Two other genes involved in sphingolipid biosynthesis (LCB2 and SUR2) were found to contain PDREs in their promoters and to be induced by the Pdr pathway. These data demonstrate extensive coordinate control of sphingolipid biosynthesis and multidrug resistance in yeast.

scholarly journals Ipl1/Aurora-B is necessary for kinetochore restructuring in meiosis I in Saccharomyces cerevisiae

2015 ◽  
Vol 26 (17) ◽  
pp. 2986-3000 ◽  
Author(s):  
Régis E. Meyer ◽  
Hoa H. Chuong ◽  
Marrett Hild ◽  
Christina L. Hansen ◽  
Michael Kinter ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Saccharomyces Cerevisiae ◽  
Protein Kinase ◽  
Mitotic Cycle ◽  
Budding Yeast ◽  
Aurora B ◽  
Quantitative Mass Spectrometry ◽  
Homologous Chromosomes ◽  
Restructuring Process ◽  
Meiosis I

In mitosis, the centromeres of sister chromosomes are pulled toward opposite poles of the spindle. In meiosis I, the opposite is true: the sister centromeres move together to the same pole, and the homologous chromosomes are pulled apart. This change in segregation patterns demands that between the final mitosis preceding meiosis and the first meiotic division, the kinetochores must be restructured. In budding yeast, unlike mammals, kinetochores are largely stable throughout the mitotic cycle. In contrast, previous work with budding and fission yeast showed that some outer kinetochore proteins are lost in early meiosis. We use quantitative mass spectrometry methods and imaging approaches to explore the kinetochore restructuring process that occurs in meiosis I in budding yeast. The Ndc80 outer kinetochore complex, but not other subcomplexes, is shed upon meiotic entry. This shedding is regulated by the conserved protein kinase Ipl1/Aurora-B and promotes the subsequent assembly of a kinetochore that will confer meiosis-specific segregation patterns on the chromosome.

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