scholarly journals The CCR4 gene from Saccharomyces cerevisiae is required for both nonfermentative and spt-mediated gene expression.

Genetics ◽  
1990 ◽  
Vol 124 (2) ◽  
pp. 283-291 ◽  
Author(s):  
C L Denis ◽  
T Malvar

Abstract Mutations in the yeast CCR4 gene inhibit expression of the glucose-repressible alcohol dehydrogenase (ADH2), as well as other nonfermentative genes, and suppress increased ADH2 expression caused by the cre1 and cre2 alleles. Both the cre1 and ccr4 alleles were shown to affect ADH II enzyme activity by altering the levels of ADH2 mRNA. Mutations in either CRE1 or CRE2 bypassed the inhibition of ADH2 expression caused by delta insertions at the ADH2 promoter which displace the ADH2 activation sequences 336 bp upstream of the TATA element. These cre1 and cre2 effects were suppressible by the ccr4 allele. The cre1 and ccr4 mutations also affected ADH2 expression when all the ADH2 regulatory sequences upstream of the TATA element were deleted. The relationship of the CRE genes to the SPT genes, which when mutated are capable of bypassing the inhibition of HIS4 expression caused by a delta promoter insertion (his4-912 delta allele), was examined. Both the cre1 and cre2 mutations allowed his4-912 delta expression. ccr4 mutations were able to suppress the ability of the cre alleles to increase his4-912 delta expression. CRE2 was shown to be allelic to the SPT6 gene, and CRE1 was found to be allelic to SPT10. We suggest that the CRE genes comprise a general transcriptional control system in yeast that requires the function of the CCR4 gene.

Blood ◽  
1998 ◽  
Vol 92 (8) ◽  
pp. 2959-2962 ◽  
Author(s):  
Arthur Schneider ◽  
Linda Forman ◽  
Beryl Westwood ◽  
Catherine Yim ◽  
James Lin ◽  
...  

Abstract In 424 African-American and 75 white subjects, we found that the −5 (TPI 592 A→G), −8 (TPI 589 G→A), and −24 (TPI 573 T→G) variants in the triosephosphate isomerase (TPI) gene occurred frequently (41.0%) in the African-American subjects but did not occur in the whites. These data suggest that this set of polymorphisms may turn out to be one of the higher-incidence molecular markers of African lineage, a surprising finding because others had reported that these nucleotide substitutions were restricted to a small subset of African Americans who had been characterized as TPI-deficiency heterozygotes. Additionally, we investigated the relationship of these variants to TPI-enzyme activity. Although the variant substitutions (occurring in three haplotypes: −5 alone, −5 −8, and −5 −8 −24) were associated with moderate reduction in enzyme activity, severe-deficiency heterozygotes could not be identified with certainty, and none of the haplotypes were restricted to subjects with marked reduction of enzyme activity. Three subjects were homozygous for the −5 −8 haplotype, a finding inconsistent with the putative role of this haplotype as the cause of a null variant incompatible with life in homozygotes. Despite these findings, the possibility remains that the −5 −8 or −5 −8 −24 haplotypes may in some instances contribute to compound heterozygosity and clinical TPI deficiency. © 1998 by The American Society of Hematology.


1996 ◽  
pp. 467-473
Author(s):  
T. Bykova ◽  
A. Sominskaya ◽  
I. Stuif ◽  
N. Anikina ◽  
A. Zaritskey

2018 ◽  
Vol 65 ◽  
pp. 299-315
Author(s):  
Claudio Scazzocchio

John Pateman was a distinguished British microbial geneticist. He came from a working-class area of London and a non-academic background. His earliest contribution to genetics was the discovery (together with John Fincham) of intracistronic complementation, an important phenomenon to understand the relationship of genetic information and protein structure; this at a time when the actual coding relationships of DNA and proteins were not yet worked out. Later on, he and his students made a fundamental contribution to the understanding of control of gene expression in eukaryotic microorganisms, providing some of the earliest examples of positive control. This work also led to the discovery of a new enzyme cofactor, the only one discovered through purely genetic evidence. He worked at various universities in Britain and Australia and trained a number of students who further developed the subject.


1990 ◽  
Vol 259 (4) ◽  
pp. L185-L197
Author(s):  
B. R. Stripp ◽  
J. A. Whitsett ◽  
D. L. Lattier

Gene transcription is regulated by the formation of protein-DNA complexes that influence the rate of specific initiation of transcription by RNA polymerase. Recent experimental advances allowing the identification of cis regulatory sequences that specify the binding of trans acting protein factors have made significant contributions to our understanding of the mechanistic complexities of transcriptional regulation. These methodologies have prompted the use of similar strategies to elucidate transcriptional control mechanisms involved in the tissue specific and developmental regulation of pulmonary surfactant protein gene expression. The purpose of this review is to describe various methodologies by which molecular biologists identify and subsequently assay regions of nucleic acids presumed to be integral in gene regulation at the level of transcription. It is well established that genes encoding surfactant proteins are subject to regulation by hormones, cytokines, and a variety of biologically active reagents. Perhaps future studies utilizing molecular tools outlined in this review will be valuable in identification of DNA sequences and protein factors required for the regulation of lung surfactant genes.


2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Ting Wang ◽  
Shu-chong Mei ◽  
Rong Fu ◽  
Hua-quan Wang ◽  
Zong-hong Shao

Abnormal telomere attrition has been found to be closely related to patients with SAA in recent years. To identify the incidence of telomere attrition in SAA patients and investigate the relationship of telomere length with clinical parameters, SAA patients(n=27)and healthy controls(n=15)were enrolled in this study. Telomere length of PWBCs was significantly shorter in SAA patients than in controls. Analysis of gene expression of Shelterin complex revealed markedly low levels ofPOT1expression in SAA groups relative to controls. No differences in the gene expression of the other Shelterin components—TRF1,TRF2,TIN2,TPP1, andRAP1—were identified. Addition of IFN-γto culture media induced a similar fall in POT1 expression in bone marrow cells to that observed in cells cultured in the presence of SAA serum, suggesting IFN-γis the agent responsible for this effect of SAA serum. Furthermore, ATR, phosphorylated ATR, and phosphorylated ATM/ATR substrate were all found similarly increased in bone marrow cells exposed to SAA serum, TNF-α, or IFN-γ. In summary, SAA patients have short telomeres and decreased POT1 expression. TNF-αand IFN-γare found at high concentrations in SAA patients and may be the effectors that trigger apoptosis through POT1 and ATR.


Genome ◽  
2014 ◽  
Vol 57 (3) ◽  
pp. 181-184 ◽  
Author(s):  
Gregory S. Downs ◽  
Christophe Liseron-Monfils ◽  
Lewis N. Lukens

Transcriptional control is an important determinant of plant development, and distinct modules of coordinated genes characterize the maize developmental transcriptome. Upstream regulatory sequences are often the primary factors that control gene expression pattern and abundance. Here, we identify 244 regulatory motifs that are significantly enriched within 24 gene expression modules previously constructed from transcript abundances of 34 876 Zea mays (maize) gene models from embryogenesis to senescence. Within modules, we identify motifs that have not been characterized. In addition, we identify motifs similar to experimentally verified motifs, and the functions of these motifs overlap with predicted module functions. This work demonstrates the power of transcript-level coexpression modules to identify both variants of known regulatory motifs and novel motifs that control a species’ developmental transcriptome.


2008 ◽  
Vol 7 (12) ◽  
pp. 2061-2068 ◽  
Author(s):  
Raymond Wightman ◽  
Rachel Bell ◽  
Richard J. Reece

ABSTRACT In Saccharomyces cerevisiae, the GAL genes encode the enzymes required for galactose metabolism. Regulation of these genes has served as the paradigm for eukaryotic transcriptional control over the last 50 years. The switch between inert and active gene expression is dependent upon three proteins—the transcriptional activator Gal4p, the inhibitor Gal80p, and the ligand sensor Gal3p. Here, we present a detailed spatial analysis of the three GAL regulatory proteins produced from their native genomic loci. Using a novel application of photobleaching, we demonstrate, for the first time, that the Gal3p ligand sensor enters the nucleus of yeast cells in the presence of galactose. Additionally, using Förster resonance energy transfer, we show that the interaction between Gal3p and Gal80p occurs throughout the yeast cell. Taken together, these data challenge existing models for the cellular localization of the regulatory proteins during the induction of GAL gene expression by galactose and suggest a mechanism for the induction of the GAL genes in which galactose-bound Gal3p moves from the cytoplasm to the nucleus to interact with the transcriptional inhibitor Gal80p.


2011 ◽  
Vol 11 (3) ◽  
pp. 334-342 ◽  
Author(s):  
Dariusz Abramczyk ◽  
Stacey Holden ◽  
Christopher J. Page ◽  
Richard J. Reece

ABSTRACT The regulation of the Saccharomyces cerevisiae GAL genes in response to galactose as a source of carbon has served as a paradigm for eukaryotic transcriptional control over the last 50 years. Three proteins—a transcriptional activator (Gal4p), an inhibitor (Gal80p), and a ligand sensor (Gal3p)—control the switch between inert and active gene expression. The molecular mechanism by which the recognition of galactose within the cell is converted into a transcriptional response has been the subject of considerable debate. In this study, using a novel and powerful method of localizing active transcription factors within the nuclei of cells, we show that a short-lived complex between Gal4p, Gal80p, and Gal3p occurs soon after the addition of galactose to cells to activate GAL gene expression. Gal3p is subsequently replaced in this complex by Gal1p, and a Gal4p-Gal80p-Gal1p complex is responsible for the continued expression of the GAL genes. The transient role of the ligand sensor indicates that current models for the induction and continued expression of the yeast GAL genes need to be reevaluated.


1984 ◽  
Vol 4 (5) ◽  
pp. 947-955 ◽  
Author(s):  
G Chisholm ◽  
T Cooper

We have isolated three cis-dominant mutations which dramatically enhance DUR1 ,2 gene expression in Saccharomyces cerevisiae. The mutant phenotype, which is expressed both in haploid and MATa/MAT alpha diploid strains, does not appear to be an alteration of the normal control system for this gene because its expression remained fully inducible and sensitive to nitrogen catabolite repression. Instead, we found much higher levels of DUR1 ,2-specific RNA under both uninduced and induced conditions, i.e., the overproduction trait was superimposed on normal regulation of the gene. The mutations seemed to affect gene expression in a unidirectional manner or to be specific for DUR1 ,2 gene expression, because other genes in proximity to the mutations were not affected. We feel that these mutations may alter the chromatin structure in the vicinity of the DUR1 ,2 upstream control sequences or, alternatively, may be Ty insertions which no longer possess the ROAM characteristics reported by others and ourselves.


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