scholarly journals A fibroblast-specific factor binds to an upstream negative control element in the promoter of the mouse alpha 1(I) collagen gene.

1991 ◽  
Vol 266 (12) ◽  
pp. 7382-7387
Author(s):  
R Ravazzolo ◽  
G Karsenty ◽  
B de Crombrugghe
Keyword(s):  
Negative Control ◽  
Control Element ◽  
Specific Factor ◽  
Collagen Gene

A negative control element in the promoter of ? 1(I) collagen gene

1990 ◽  
Vol 14 ◽  
pp. 50
Author(s):  
R RAVAZZOLO ◽  
G KARSENTY ◽  
B DECROMBRUGGHE
Keyword(s):  
Negative Control ◽  
Control Element ◽  
Collagen Gene

scholarly journals The Iron Control Element, Acting in Positive and Negative Control of Iron-Regulated Bradyrhizobium japonicum Genes, Is a Target for the Irr Protein

2006 ◽  
Vol 188 (6) ◽  
pp. 2294-2294 ◽  
Author(s):  
G. Rudolph ◽  
G. Semini ◽  
F. Hauser ◽  
A. Lindemann ◽  
M. Friberg ◽  
...  
Keyword(s):  
Bradyrhizobium Japonicum ◽  
Negative Control ◽  
Control Element

scholarly journals Insulin gene expression in nonexpressing cells appears to be regulated by multiple distinct negative-acting control elements.

1991 ◽  
Vol 11 (5) ◽  
pp. 2881-2886 ◽  
Author(s):  
S R Cordle ◽  
J Whelan ◽  
E Henderson ◽  
H Masuoka ◽  
P A Weil ◽  
...  
Keyword(s):  
Pancreatic Beta Cells ◽  
Negative Control ◽  
Insulin Gene ◽  
Control Element ◽  
Cell Type ◽  
Specific Expression ◽  
Sequence Element ◽  
Enhancer Element ◽  
Cell Type Specific ◽  
Specific Regulation

Selective transcription of the insulin gene in pancreatic beta cells is regulated by its enhancer, located between nucleotides -340 and -91 relative to the transcription start site. Transcription from the enhancer is controlled by both positive- and negative-acting cellular factors. Cell-type-specific expression is mediated principally by a single cis-acting enhancer element located between -100 and -91 in the rat insulin II gene (referred to as the insulin control element [ICE]), which is acted upon by both of these cellular activities. Analysis of the effect of 5' deletions within the insulin enhancer has identified a region between nucleotides -217 and -197 that is also a site of negative control. Deletion of these sequences from the 5' end of the enhancer leads to transcription of the enhancer in non-insulin-producing cells, even though the ICE is intact. Derepression of this ICE-mediated effect was shown to be due to the binding of a ubiquitously distributed cellular factor to a sequence element which resides just upstream of the ICE (i.e., between nucleotides -110 and -100). We discuss the possible relationship of these results to cell-type-specific regulation of the insulin gene.

scholarly journals Positive Control of Swarming, Rhamnolipid Synthesis, and Lipase Production by the Posttranscriptional RsmA/RsmZ System in Pseudomonas aeruginosa PAO1

2004 ◽  
Vol 186 (10) ◽  
pp. 2936-2945 ◽  
Author(s):  
Karin Heurlier ◽  
Faye Williams ◽  
Stephan Heeb ◽  
Corinne Dormond ◽  
Gabriella Pessi ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Target Genes ◽  
Rna Binding ◽  
Regulatory Protein ◽  
Lipase Production ◽  
Positive Control ◽  
Negative Control ◽  
Control Element ◽  
Signal Molecules ◽  
Positive Effects

ABSTRACT In Pseudomonas aeruginosa, the small RNA-binding, regulatory protein RsmA is a negative control element in the formation of several extracellular products (e.g., pyocyanin, hydrogen cyanide, PA-IL lectin) as well as in the production of N-acylhomoserine lactone quorum-sensing signal molecules. RsmA was found to control positively the ability to swarm and to produce extracellular rhamnolipids and lipase, i.e., functions contributing to niche colonization by P. aeruginosa. An rsmA null mutant was entirely devoid of swarming but produced detectable amounts of rhamnolipids, suggesting that factors in addition to rhamnolipids influence the swarming ability of P. aeruginosa. A small regulatory RNA, rsmZ, which antagonized the effects of RsmA, was identified in P. aeruginosa. Expression of the rsmZ gene was dependent on both the global regulator GacA and RsmA, increased with cell density, and was subject to negative autoregulation. Overexpression of rsmZ and a null mutation in rsmA resulted in quantitatively similar, negative or positive effects on target genes, in agreement with a model that postulates titration of RsmA protein by RsmZ RNA.

Insulin gene expression in nonexpressing cells appears to be regulated by multiple distinct negative-acting control elements

1991 ◽  
Vol 11 (5) ◽  
pp. 2881-2886
Author(s):  
S R Cordle ◽  
J Whelan ◽  
E Henderson ◽  
H Masuoka ◽  
P A Weil ◽  
...  
Keyword(s):  
Pancreatic Beta Cells ◽  
Negative Control ◽  
Insulin Gene ◽  
Control Element ◽  
Cell Type ◽  
Specific Expression ◽  
Sequence Element ◽  
Enhancer Element ◽  
Cell Type Specific ◽  
Specific Regulation

Selective transcription of the insulin gene in pancreatic beta cells is regulated by its enhancer, located between nucleotides -340 and -91 relative to the transcription start site. Transcription from the enhancer is controlled by both positive- and negative-acting cellular factors. Cell-type-specific expression is mediated principally by a single cis-acting enhancer element located between -100 and -91 in the rat insulin II gene (referred to as the insulin control element [ICE]), which is acted upon by both of these cellular activities. Analysis of the effect of 5' deletions within the insulin enhancer has identified a region between nucleotides -217 and -197 that is also a site of negative control. Deletion of these sequences from the 5' end of the enhancer leads to transcription of the enhancer in non-insulin-producing cells, even though the ICE is intact. Derepression of this ICE-mediated effect was shown to be due to the binding of a ubiquitously distributed cellular factor to a sequence element which resides just upstream of the ICE (i.e., between nucleotides -110 and -100). We discuss the possible relationship of these results to cell-type-specific regulation of the insulin gene.

scholarly journals Pheromone-Regulated Expression of Sex Pheromone Plasmid pAD1-Encoded Aggregation Substance Depends on at Least Six Upstream Genes and a cis-Acting, Orientation-Dependent Factor

2000 ◽  
Vol 182 (13) ◽  
pp. 3816-3825 ◽  
Author(s):  
Albrecht B. Muscholl-Silberhorn
Keyword(s):  
Sex Pheromone ◽  
Amylase Activity ◽  
Constitutive Expression ◽  
Negative Control ◽  
Control Element ◽  
Cell Contact ◽  
Dependent Manner ◽  
Cis Acting ◽  
Aggregation Substance ◽  
Dependent Factor

ABSTRACT Conjugative transfer of Enterococcus faecalis-specific sex pheromone plasmids relies on an adhesin, called aggregation substance, to confer a tight cell-to-cell contact between the mating partners. To analyze the dependence of pAD1-encoded aggregation substance, Asa1, on pheromone induction, a variety of upstream fragments were fused to an α-amylase reporter gene, amyL, by use of a novel promoter probe vector, pAMY-em1. For pheromone-regulated α-amylase activity, a total of at least six genes, traB, traC, traA,traE1, orfY, and orf1, are required: TraB efficiently represses asa1 (by a mechanism unrelated to its presumptive function in pheromone shutdown, since a complete shutdown is observed exclusively in the presence oftraC); only traC can relievetraB-mediated repression in a pheromone-dependent manner. In addition to traB, traA is required but not sufficient for negative control. Mutational inactivation oftraE1, orfY, or orf1, respectively, results in a total loss of α-amylase activity for constructs normally mediating constitutive expression. Inversion of a fragment coveringtraA, P0, and traE1 without disrupting any gene or control element switches off amyL orasa1 expression, indicating the involvement of acis-acting, orientation-dependent factor (as had been shown for plasmid pCF10). Unexpectedly, pAD1 represses all pAMY-em1 derivatives in trans, while its own pheromone-dependent functions are unaffected. The discrepancy between the new data and those of former studies defining TraE1 as a trans-acting positive regulator is discussed.

scholarly journals IDENTIFICATION OF NEW GENES INVOLVED IN THE REGULATION OF YEAST ALCOHOL DEHYDROGENASE II

Genetics ◽  
1984 ◽  
Vol 108 (4) ◽  
pp. 833-844
Author(s):  
Clyde L Denis
Keyword(s):  
Alcohol Dehydrogenase ◽  
Positive Control ◽  
Negative Control ◽  
Control Element ◽  
Wild Type ◽  
Yeast Alcohol Dehydrogenase ◽  
Recessive Mutations ◽  
New Genes

ABSTRACT Recessive mutations in two negative control elements, CRE1 and CRE2, have been obtained that allow the glucose-repressible alcohol dehydrogenase (ADHII) of yeast to escape repression by glucose. Both the cre1 and cre2 alleles affected ADHII synthesis irrespective of the allele of the positive effector, ADR1. However, for complete derepression of ADHII synthesis, a wild-type ADR1 gene was required. Neither the cre1 nor cre2 alleles affected the expression of several other glucose-repressible enzymes. A third locus, CCR4, was identified by recessive mutations that suppressed the cre1 and cre2 phenotypes. The ccr4 allele blocked the derepression of ADHII and several other glucose-repressible enzymes, indicating that the CCR4 gene is a positive control element. The ccr4 allele had no effect on the repression of ADHII when it was combined with the ADR1-5  c allele, whereas the phenotypically similar ccr1 allele, which partially suppresses ADR1-5  c, did not suppress the cre1 or cre2 phenotype. Complementation studies also indicated that ccr1 and snf1 are allelic. A model of ADHII regulation is proposed in which both ADR1 and CCR4 are required for ADHII expression. CRE1 and CRE2 negatively control CCR4, whereas CCR1 is required for ADR1 function.

Binding of multiple nuclear factors to the 5' upstream regulatory element of the murine major histocompatibility class I gene

1987 ◽  
Vol 7 (12) ◽  
pp. 4542-4548
Author(s):  
Y Shirayoshi ◽  
J Miyazaki ◽  
P A Burke ◽  
K Hamada ◽  
E Appella ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Protein Interactions ◽  
Regulatory Element ◽  
Negative Control ◽  
Class I ◽  
Control Element ◽  
Major Histocompatibility ◽  
Nucleotide Substitutions ◽  
Mobility Shift ◽  
Histocompatibility Complex

Transcription of mouse major histocompatibility complex class I genes is controlled by the conserved class I regulatory element (CRE) in the 5' flanking region. The CRE, approximately 40 base pairs long, acts as a negative control element in undifferentiated F9 embryonal carcinoma cells which do not express the major histocompatibility complex genes. The same element, however, acts as a positive control element in cells expressing the genes at high levels. To investigate the molecular basis of the regulatory role of the CRE, we studied the binding of nuclear proteins to the CRE of the H-2Ld gene by gel mobility shift and methylation interference experiments. Nuclear extracts from L fibroblasts and LH8 T lymphocytes revealed three distinct factors that bind discrete sequences within the CRE. The three sequences correspond to the inverted and direct repeats within the CRE. In contrast, F9 extracts exhibited factor binding to only two of the three sequences and lack a major factor detected in the above two cell types. Protein-binding sites within each of the three sequences were identified by methylation interference experiments. These data were in full agreement with results obtained by a competition assay performed with a series of mutant oligonucleotides containing a few nucleotide substitutions in each of the three regions. The results illustrate complex DNA-protein interactions in which several independent proteins bind to overlapping sequences in the CRE in a cell type-specific fashion.

scholarly journals Binding of multiple nuclear factors to the 5' upstream regulatory element of the murine major histocompatibility class I gene.

1987 ◽  
Vol 7 (12) ◽  
pp. 4542-4548 ◽  
Author(s):  
Y Shirayoshi ◽  
J Miyazaki ◽  
P A Burke ◽  
K Hamada ◽  
E Appella ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Protein Interactions ◽  
Regulatory Element ◽  
Negative Control ◽  
Class I ◽  
Control Element ◽  
Major Histocompatibility ◽  
Nucleotide Substitutions ◽  
Mobility Shift ◽  
Histocompatibility Complex

Transcription of mouse major histocompatibility complex class I genes is controlled by the conserved class I regulatory element (CRE) in the 5' flanking region. The CRE, approximately 40 base pairs long, acts as a negative control element in undifferentiated F9 embryonal carcinoma cells which do not express the major histocompatibility complex genes. The same element, however, acts as a positive control element in cells expressing the genes at high levels. To investigate the molecular basis of the regulatory role of the CRE, we studied the binding of nuclear proteins to the CRE of the H-2Ld gene by gel mobility shift and methylation interference experiments. Nuclear extracts from L fibroblasts and LH8 T lymphocytes revealed three distinct factors that bind discrete sequences within the CRE. The three sequences correspond to the inverted and direct repeats within the CRE. In contrast, F9 extracts exhibited factor binding to only two of the three sequences and lack a major factor detected in the above two cell types. Protein-binding sites within each of the three sequences were identified by methylation interference experiments. These data were in full agreement with results obtained by a competition assay performed with a series of mutant oligonucleotides containing a few nucleotide substitutions in each of the three regions. The results illustrate complex DNA-protein interactions in which several independent proteins bind to overlapping sequences in the CRE in a cell type-specific fashion.

scholarly journals Activation of a muscle-specific actin gene promoter in serum-stimulated fibroblasts.

1992 ◽  
Vol 3 (10) ◽  
pp. 1073-1083 ◽  
Author(s):  
E S Stoflet ◽  
L J Schmidt ◽  
P K Elder ◽  
G M Korf ◽  
D N Foster ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Gene Promoter ◽  
Negative Control ◽  
Control Element ◽  
Deletion Mapping ◽  
Actin Gene ◽  
Cis Acting ◽  
Beta Actin ◽  
Actin Promoter ◽  
Alpha Actin

Treatment of AKR-2B mouse fibroblasts with serum growth factors or inhibitors of protein synthesis, such as cycloheximide, results in a stimulation of cytoskeletal beta-actin transcription but has no effect on transcription of muscle-specific isotypes, such as the vascular smooth muscle (VSM) alpha-actin gene. Deletion mapping and site-specific mutagenesis studies demonstrated that a single "CArG" element of the general form CC(A/T)6GG was necessary and possibly sufficient to impart serum and cycloheximide-inducibility to the beta-actin promoter. Although the VSM alpha-actin promoter exhibits at least three similar sequence elements, it remained refractory to serum and cycloheximide induction. However, deletion of a 33 base pair sequence between -191 and -224 relative to the transcription start site resulted in the transcriptional activation of this muscle-specific promoter in rapidly growing or serum-stimulated fibroblasts. Although the activity of this truncated promoter was potentiated by cycloheximide in a manner indistinguishable from that of the beta-actin promoter, this was dependent on a more complex array of interacting elements. These included at least one CArG box and a putative upstream activating element closely associated with the -191 to -224 inhibitory sequences. These results demonstrate that the expression of a muscle-specific actin gene in fibroblasts is suppressed by a cis-acting negative control element and that in the absence of this element, the promoter is responsive to growth factor-induced signal transduction pathways.

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