RPD3 encodes a second factor required to achieve maximum positive and negative transcriptional states in Saccharomyces cerevisiae

1991 ◽  
Vol 11 (12) ◽  
pp. 6317-6327 ◽  
Author(s):  
M Vidal ◽  
R F Gaber
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Target Genes ◽  
Current Data ◽  
Regulatory Function ◽  
Fourfold Increase ◽  
Recessive Mutations ◽  
Activation Of Transcription ◽  
Transcriptional Regulatory ◽  
Low Levels ◽  
Full Activation

In Saccharomyces cerevisiae, TRK1 and TRK2 encode the high- and low-affinity K+ transporters, respectively. In cells containing a deletion of TRK1, transcription levels of TRK2 are extremely low and are limiting for growth in media containing low levels of K+ (Trk- phenotype). Recessive mutations in RPD1 and RPD3 suppress the TRK2, conferring an approximately fourfold increase in transcription. rpd3 mutations confer pleiotropic phenotypes, including (i) mating defects, (ii) hypersensitivity to cycloheximide, (iii) inability to sporulate as homozygous diploids, and (iv) constitutive derepression of acid phosphatase. RPD3 was cloned and is predicted to encode a 48-kDa protein with no extensive similarity to proteins contained in current data bases. Deletion of RPD3 is not lethal but confers phenotypes identical to those caused by spontaneous mutations. RPD3 is required for both full repression and full activation of transcription of target genes including PHO5, STE6, and TY2. RPD3 is the second gene required for this function, since RPD1 is also required. The effects of mutations in RPD1 and RPD3 are not additive, suggesting that these genes are involved in the same transcriptional regulatory function or pathway.

scholarly journals RPD3 encodes a second factor required to achieve maximum positive and negative transcriptional states in Saccharomyces cerevisiae.

1991 ◽  
Vol 11 (12) ◽  
pp. 6317-6327 ◽  
Author(s):  
M Vidal ◽  
R F Gaber
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Target Genes ◽  
Current Data ◽  
Regulatory Function ◽  
Fourfold Increase ◽  
Recessive Mutations ◽  
Activation Of Transcription ◽  
Transcriptional Regulatory ◽  
Low Levels ◽  
Full Activation

In Saccharomyces cerevisiae, TRK1 and TRK2 encode the high- and low-affinity K+ transporters, respectively. In cells containing a deletion of TRK1, transcription levels of TRK2 are extremely low and are limiting for growth in media containing low levels of K+ (Trk- phenotype). Recessive mutations in RPD1 and RPD3 suppress the TRK2, conferring an approximately fourfold increase in transcription. rpd3 mutations confer pleiotropic phenotypes, including (i) mating defects, (ii) hypersensitivity to cycloheximide, (iii) inability to sporulate as homozygous diploids, and (iv) constitutive derepression of acid phosphatase. RPD3 was cloned and is predicted to encode a 48-kDa protein with no extensive similarity to proteins contained in current data bases. Deletion of RPD3 is not lethal but confers phenotypes identical to those caused by spontaneous mutations. RPD3 is required for both full repression and full activation of transcription of target genes including PHO5, STE6, and TY2. RPD3 is the second gene required for this function, since RPD1 is also required. The effects of mutations in RPD1 and RPD3 are not additive, suggesting that these genes are involved in the same transcriptional regulatory function or pathway.

scholarly journals Spatial organization of the transcriptional regulatory network of Saccharomyces cerevisiae

2019 ◽  
Author(s):  
Dong-Qing Sun ◽  
Liu Tian ◽  
Bin-Guang Ma
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Regulatory Network ◽  
Spatial Organization ◽  
Target Genes ◽  
Transcriptional Regulatory Network ◽  
3D Structure ◽  
Three Dimensional ◽  
3D Genome ◽  
Transcriptional Regulatory ◽  
Four Levels

AbstractTranscriptional regulatory network (TRN) is a directed complex network composed of all regulatory interactions between transcription factors and corresponding target genes. Recently, the three-dimensional (3D) genomics studies have shown that the 3D structure of the genome makes a difference to the regulation of gene transcription, which provides us with a novel perspective. In this study, we constructed the TRN of the budding yeast Saccharomyces cerevisiae and placed it in the context of 3D genome model. We analyzed the spatial organization of the yeast TRN on four levels: global feature, central nodes, hierarchical structure and network motifs. Our results suggested that the TRN of S. cerevisiae presents an optimized structure in space to adapt to functional requirement.

GENES AFFECTING THE REGULATION OF SUC2 GENE EXPRESSION BY GLUCOSE REPRESSION IN SACCHAROMYCES CEREVISIAE

Genetics ◽  
1984 ◽  
Vol 108 (4) ◽  
pp. 845-858
Author(s):  
Lenore Neigeborn ◽  
Marian Carlson
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Glucose Repression ◽  
Invertase Activity ◽  
Recessive Mutations ◽  
Glycerol Utilization ◽  
Suc2 Gene ◽  
Complementation Groups ◽  
Low Levels ◽  
High Level

ABSTRACT Mutants of Saccharomyces cerevisiae with defects in sucrose or raffinose fermentation were isolated. In addition to mutations in the SUC2 structural gene for invertase, we recovered 18 recessive mutations that affected the regulation of invertase synthesis by glucose repression. These mutations included five new snf1 (sucrose nonfermenting) alleles and also defined five new complementation groups, designated snf2, snf3, snf4, snf5 and snf6. The snf2, snf4 and snf5 mutants produced little or no secreted invertase under derepressing conditions and were pleiotropically defective in galactose and glycerol utilization, which are both regulated by glucose repression. The snf6 mutant produced low levels of secreted invertase under derepressing conditions, and no pleiotropy was detected. The snf3 mutants derepressed secreted invertase to 10-35% the wild-type level but grew less well on sucrose than expected from their invertase activity; in addition, snf3 mutants synthesized some invertase under glucose-repressing conditions.—We examined the interactions between the different snf mutations and ssn6, a mutation causing constitutive (glucose-insensitive) high-level invertase synthesis that was previously isolated as a suppressor of snf1 . The ssn6 mutation completely suppressed the defects in derepression of invertase conferred by snf1, snf3, snf4 and snf6, and each double mutant showed the constitutivity for invertase typical of ssn6 single mutants. In contrast, snf2 ssn6 and snf5 ssn6 strains produced only moderate levels of invertase under derepressing conditions and very low levels under repressing conditions. These findings suggest roles for the SNF1 through SNF6 and SSN6 genes in the regulation of SUC2 gene expression by glucose repression.

scholarly journals Investigating the mechanism of the Tup1-Cyc8 (Ssn6) Co-Repressor complex in the yeast Saccharomyces cerevisiae

2020 ◽  
Vol 2 (7A) ◽  
Author(s):  
Brenda Lee
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Stress Response ◽  
Target Genes ◽  
Nuclear Protein ◽  
Yeast Saccharomyces Cerevisiae ◽  
Sequence Of Events ◽  
Repressive Chromatin ◽  
Activation Of Transcription ◽  
Independent Functions ◽  
Repressor Complex

The Tup1-Cyc8 (Ssn6) complex is a powerful epigenetic repressor of genes in the yeast Saccharomyces cerevisiae. The highly conserved complex brings about a repressive chromatin structure at regulatory regions of its target genes or prevents the recruitment of factors needed for activation of transcription. A gap in the current understanding is whether each of the subunits contribute differently to repression. The FLO family of genes are repressed by the Tup1-Cyc8 complex, these genes encode the proteins required for flocculation, a stress response in yeast where the cells aggregate, or form flocs, to protect cells within the floc. Interestingly, each mutant strain has a distinct flocculant phenotype. The tup1Δ strain displays large, dense flocs compared to smaller, more dispersed flocs associated with the cyc8Δ strain. RT-qPCR showed that FLO1 is highly de-repressed in the tup1Δ strain whereas it is de-repressed to a significantly lower level in the cyc8Δ strain. Using the Anchor Away (AA) technique, which allows for a nuclear protein to be conditionally sequestered to the cytoplasm, I am investigating differences in the sequence of events at the FLO1 promoter when Tup1p or when Cyc8p is removed from the nucleus. Six hours after Cyc8p is removed from the nucleus transcription of FLO1 almost reaches the maximum transcription seen in the cyc8Δstrain. However, six hours after removing Tup1p the level of transcription of FLO1 is still over ten times lower than the maximum transcription in tup1Δ. This difference indicates that each of the subunits have independent functions within the complex.

scholarly journals Characterization of TRP-1 mRNA levels in dominant and recessive mutations at the mouse brown (b) locus.

Genetics ◽  
1990 ◽  
Vol 126 (2) ◽  
pp. 451-459
Author(s):  
I J Jackson ◽  
D Chambers ◽  
E M Rinchik ◽  
D C Bennett
Keyword(s):  
Mrna Levels ◽  
Wild Type ◽  
Recessive Mutations ◽  
Activation Of Transcription ◽  
Membrane Bound ◽  
The Common ◽  
Low Levels ◽  
The Relationship ◽  
Tyrosinase Related Protein

Abstract The mouse brown locus encodes a putative membrane-bound metalloenzyme, tyrosinase-related protein-1 (TRP-1). We have examined the effect on mRNA expression of the locus of a number of mutant alleles. The common null mutant allele, brown, produces wild-type levels of TRP-1 mRNA, which is nonfunctional. Another recessive allele, cordovan-Harwell, has an intermediate, dark-brown phenotype and produces only very low levels of presumably normal TRP-1 mRNA. Two dominant alleles appear to act by killing the melanocyte in which they are expressed. One of them, Light, has normal size and amounts of TRP-1 mRNA. The other, White-based brown, produces no detectable TRP-1 mRNA. It has a gross DNA rearrangement at the 5' end, and we speculate that this results in activation of transcription of sequences not usually seen in melanocytes, and that this is toxic to the cell. The relationship between phenotype and molecular structure at the locus is discussed, and we draw some general principles applicable to other developmental genes.

scholarly journals Suppressor Analysis of Mutations in the 5′-Untranslated Region of COB mRNA Identifies Components of General Pathways for Mitochondrial mRNA Processing and Decay in Saccharomyces cerevisiae

Genetics ◽  
1999 ◽  
Vol 151 (4) ◽  
pp. 1315-1325
Author(s):  
Wei Chen ◽  
Maria A Islas-Osuna ◽  
Carol L Dieckmann
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Untranslated Region ◽  
Mitochondrial Rna ◽  
Rna Turnover ◽  
Single Nucleotide ◽  
Mrna Stabilization ◽  
Recessive Mutations ◽  
A Subunit ◽  
Suppressor Analysis ◽  
Dominant Suppressor

Abstract The cytochrome b gene in Saccharomyces cerevisiae, COB, is encoded by the mitochondrial genome. Nuclear-encoded Cbp1 protein is required specifically for COB mRNA stabilization. Cbp1 interacts with a CCG element in a 64-nucleotide sequence in the 5′-untranslated region of COB mRNA. Mutation of any nucleotide in the CCG causes the same phenotype as cbp1 mutations, i.e., destabilization of both COB precursor and mature message. In this study, eleven nuclear suppressors of single-nucleotide mutations in CCG were isolated and characterized. One dominant suppressor is in CBP1, while the other 10 semidominant suppressors define five distinct linkage groups. One group of four mutations is in PET127, which is required for 5′ end processing of several mitochondrial mRNAs. Another mutation is linked to DSS1, which is a subunit of mitochondrial 3′ → 5′ exoribonuclease. A mutation linked to the SOC1 gene, previously defined by recessive mutations that suppress cbp1 ts alleles and stabilize many mitochondrial mRNAs, was also isolated. We hypothesize that the products of the two uncharacterized genes also affect mitochondrial RNA turnover.

scholarly journals Transcriptome Analysis Reveals a Promotion of Carotenoid Production by Copper Ions in Recombinant Saccharomyces cerevisiae

2021 ◽  
Vol 9 (2) ◽  
pp. 233
Author(s):  
Buli Su ◽  
Anzhang Li ◽  
Ming-Rong Deng ◽  
Honghui Zhu
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcriptome Analysis ◽  
Gene Expression Analysis ◽  
Target Genes ◽  
Copper Ions ◽  
Carotenoid Production ◽  
Carotenoid Accumulation ◽  
Nutritional Components ◽  
Differential Gene ◽  
First Time

We previously constructed a Saccharomyces cerevisiae carotenoid producer BL03-D-4 which produced much more carotenoid in YPM (modified YPD) media than YPD media. In this study, the impacts of nutritional components on carotenoid accumulation of BL03-D-4 were investigated. When using YPM media, the carotenoid yield was increased 10-fold compared to using the YPD media. To elucidate the hidden mechanism, a transcriptome analysis was performed and showed that 464 genes changed significantly in YPM media. Furthermore, inspired by the differential gene expression analysis which indicated that ADY2, HES1, and CUP1 showed the most remarkable changes, we found that the improvement of carotenoid accumulation in YPM media was mainly due to the copper ions, since supplementation of 0.08 mM CuSO4 in YPD media could increase carotenoid yield 9.2-fold. Reverse engineering of target genes was performed and carotenoid yield could be increased 6.4-fold in YPD media through overexpression of ACE1. The present study revealed for the first time the prominent promotion of carotenoid yield by copper ions in engineered S. cerevisiae and provided a new target ACE1 for genetic engineering of S. cerevisiae for the bioproduction of carotenoids.

scholarly journals Differential activation mechanisms of two isoforms of Gcr1 transcription factor generated from spliced and un-spliced transcripts in Saccharomyces cerevisiae

2020 ◽  
Author(s):  
Seungwoo Cha ◽  
Chang Pyo Hong ◽  
Hyun Ah Kang ◽  
Ji-Sook Hahn
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcription Factor ◽  
Target Genes ◽  
Gene Encoding ◽  
Metabolic Switch ◽  
Differential Activation ◽  
N Terminus ◽  
Activation Mechanisms ◽  
In Trans ◽  
Separate Activation

Abstract Gcr1, an important transcription factor for glycolytic genes in Saccharomyces cerevisiae, was recently revealed to have two isoforms, Gcr1U and Gcr1S, produced from un-spliced and spliced transcripts, respectively. In this study, by generating strains expressing only Gcr1U or Gcr1S using the CRISPR/Cas9 system, we elucidate differential activation mechanisms of these two isoforms. The Gcr1U monomer forms an active complex with its coactivator Gcr2 homodimer, whereas Gcr1S acts as a homodimer without Gcr2. The USS domain, 55 residues at the N-terminus existing only in Gcr1U, inhibits dimerization of Gcr1U and even acts in trans to inhibit Gcr1S dimerization. The Gcr1S monomer inhibits the metabolic switch from fermentation to respiration by directly binding to the ALD4 promoter, which can be restored by overexpression of the ALD4 gene, encoding a mitochondrial aldehyde dehydrogenase required for ethanol utilization. Gcr1U and Gcr1S regulate almost the same target genes, but show unique activities depending on growth phase, suggesting that these isoforms play differential roles through separate activation mechanisms depending on environmental conditions.

scholarly journals Genomic Approach to Identification of Mutations Affecting Caspofungin Susceptibility in Saccharomyces cerevisiae

2004 ◽  
Vol 48 (10) ◽  
pp. 3871-3876 ◽  
Author(s):  
Sarit Markovich ◽  
Aya Yekutiel ◽  
Itamar Shalit ◽  
Yona Shadkchan ◽  
Nir Osherov
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Wall ◽  
Ergosterol Biosynthesis ◽  
Membrane Function ◽  
Minimum Effective Concentration ◽  
Fourfold Increase ◽  
Microdilution Method ◽  
New Genes ◽  
Broth Microdilution Method ◽  
Glucan Synthesis

ABSTRACT The antifungal agent caspofungin (CAS) specifically interferes with glucan synthesis and cell wall formation. To further study the cellular processes affected by CAS, we analyzed a Saccharomyces cerevisiae mutant collection (4,787 individual knockout mutations) to identify new genes affecting susceptibility to the drug. This collection was screened for increased CAS sensitivity (CAS-IS) or increased CAS resistance (CAS-IR). MICs were determined by the broth microdilution method. Disruption of 20 genes led to CAS-IS (four- to eightfold reductions in the MIC). Eleven of the 20 genes are involved in cell wall and membrane function, notably in the protein kinase C (PKC) integrity pathway (MID2, FKS1, SMI1, and BCK1), chitin and mannan biosynthesis (CHS3, CHS4, CHS7, and MNN10), and ergosterol biosynthesis (ERG5 and ERG6). Four of the 20 genes (TPO1, VPS65, VPS25, and CHC1) are involved in vacuole and transport functions, 3 of the 20 genes (CCR4, POP2, and NPL3) are involved in the control of transcription, and 2 of the 20 genes are of unknown function. Disruption of nine additional genes led to CAS-IR (a fourfold increase of MIC). Five of these nine genes (SLG1, ERG3, VRP1, CSG2, and CKA2) are involved in cell wall function and signal transduction, and two of the nine genes (VPS67 and SAC2) are involved in vacuole function. To assess the specificity of susceptibility to CAS, the MICs of amphotericin B, fluconazole, flucytosine, and calcofluor for the strains were tested. Seven of 20 CAS-IS strains (with disruption of FKS1, SMI1, BCK1, CHS4, ERG5, TPO1, and ILM1) and 1 of 9 CAS-IR strains (with disruption of SLG1) demonstrated selective susceptibility to CAS. To further explore the importance of PKC in CAS susceptibility, the activity of the PKC inhibitor staurosporine in combination with CAS was tested against eight Aspergillus clinical isolates by the microdilution assay. Synergistic or synergistic-to-additive activities were found against all eight isolates by use of both MIC and minimum effective concentration endpoints.

scholarly journals Screening Driving Transcription Factors in the Processing of Gastric Cancer

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Guangzhong Xu ◽  
Kai Li ◽  
Nengwei Zhang ◽  
Bin Zhu ◽  
Guosheng Feng
Keyword(s):  
Gastric Cancer ◽  
Transcription Factors ◽  
Regulatory Network ◽  
Target Genes ◽  
Transcriptional Regulatory Network ◽  
Expression Profiles ◽  
Functional Enrichment ◽  
Regulatory Mechanisms ◽  
Integrated Analysis ◽  
Transcriptional Regulatory

Background. Construction of the transcriptional regulatory network can provide additional clues on the regulatory mechanisms and therapeutic applications in gastric cancer.Methods. Gene expression profiles of gastric cancer were downloaded from GEO database for integrated analysis. All of DEGs were analyzed by GO enrichment and KEGG pathway enrichment. Transcription factors were further identified and then a global transcriptional regulatory network was constructed.Results. By integrated analysis of the six eligible datasets (340 cases and 43 controls), a bunch of 2327 DEGs were identified, including 2100 upregulated and 227 downregulated DEGs. Functional enrichment analysis of DEGs showed that digestion was a significantly enriched GO term for biological process. Moreover, there were two important enriched KEGG pathways: cell cycle and homologous recombination. Furthermore, a total of 70 differentially expressed TFs were identified and the transcriptional regulatory network was constructed, which consisted of 566 TF-target interactions. The top ten TFs regulating most downstream target genes were BRCA1, ARID3A, EHF, SOX10, ZNF263, FOXL1, FEV, GATA3, FOXC1, and FOXD1. Most of them were involved in the carcinogenesis of gastric cancer.Conclusion. The transcriptional regulatory network can help researchers to further clarify the underlying regulatory mechanisms of gastric cancer tumorigenesis.

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