Replication-independent cis-acting element of a maize histone gene promoter

Plant Science ◽  
1993 ◽  
Vol 89 (2) ◽  
pp. 177-184 ◽  
Author(s):  
Marc Lepetit ◽  
Martine Ehling ◽  
Rossitza Atanassova ◽  
Nicole Chaubet ◽  
Claude Gigot
Keyword(s):  
Gene Promoter ◽  
Histone Gene ◽  
Cis Acting

scholarly journals Characterization of cis-acting elements in the rat ATP citrate-lyase gene promoter

2002 ◽  
Vol 34 (1) ◽  
pp. 60-68 ◽  
Author(s):  
Young-An Moon ◽  
Sahng-Wook Park ◽  
Kyung-Sup Kim
Keyword(s):  
Gene Promoter ◽  
Atp Citrate Lyase ◽  
Cis Acting ◽  
Citrate Lyase

scholarly journals Identification and characterization of cis-acting elements conferring insulin responsiveness on hamster cholesterol 7α-hydroxylase gene promoter

2000 ◽  
Vol 347 (1) ◽  
pp. 147 ◽  
Author(s):  
Emma DE FABIANI ◽  
Maurizio CRESTANI ◽  
Maria MARRAPODI ◽  
Alessandra PINELLI ◽  
Viviana GOLFIERI ◽  
...  
Keyword(s):  
Gene Promoter ◽  
Cis Acting ◽  
Hydroxylase Gene ◽  
Insulin Responsiveness ◽  
Identification And Characterization

Tissue-specific transcription of the mouse alpha-fetoprotein gene promoter is dependent on HNF-1

1989 ◽  
Vol 9 (10) ◽  
pp. 4204-4212
Author(s):  
M H Feuerman ◽  
R Godbout ◽  
R S Ingram ◽  
S M Tilghman
Keyword(s):  
Specific Binding ◽  
Gene Promoter ◽  
Binding Activity ◽  
Alpha Fetoprotein ◽  
Transient Expression Assay ◽  
Band Shift ◽  
Specific Expression ◽  
Tissue Specific ◽  
Cis Acting ◽  
Dnase I Footprinting

Previous work identified four upstream cis-acting elements required for tissue-specific expression of the alpha-fetoprotein (AFP) gene: three distal enhancers and a promoter. To further define the role of the promoter in regulating AFP gene expression, segments of the region were tested for the ability to direct transcription of a reporter gene in transient expression assay. Experiments showed that the region within 250 base pairs of the start of transcription was sufficient to confer liver-specific transcription. DNase I footprinting and band shift assays indicated that the region between -130 and -100 was recognized by two factors, one of which was highly sequence specific and found only in hepatoma cells. Competition assays suggested that the liver-specific binding activity was HNF-1, previously identified by its binding to other liver-specific promoters. Mutation of the HNF-1 recognition site at -120 resulted in a significant reduction in transcription in transfection assays, suggesting a biological role for HNF-1 in the regulation of AFP expression.

Distinct regulation of the interleukin-1 and interleukin-6 response elements of the rat haptoglobin gene in rat and human hepatoma cells

1990 ◽  
Vol 10 (11) ◽  
pp. 5967-5976
Author(s):  
H Baumann ◽  
K K Morella ◽  
G P Jahreis ◽  
S Marinković
Keyword(s):  
Interleukin 1 ◽  
Gene Promoter ◽  
Cell Types ◽  
Regulatory Elements ◽  
Hepatoma Cells ◽  
Expression Vectors ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Cis Acting ◽  
Chloramphenicol Acetyltransferase Gene

The transcription rate of the haptoglobin (Hp) gene is stimulated by interleukin-1 (IL-1), IL-6, and dexamethasone in rat hepatoma (H-35) cells. To identify the cis-acting regulatory elements responsive to these hormones, various lengths of 5' Hp gene-flanking regions, including the promoter, were inserted into chloramphenicol acetyltransferase gene expression vectors and transiently introduced into H-35 cells. The first 4 kb of 5' region mediated a severalfold increase in expression after treatment with IL-6 and dexamethasone. No response to IL-1 was detectable. When, however, upstream sequences were deleted to position -165 relative to the transcription start site, a significant stimulation by IL-1 was gained without appreciably affecting the IL-6 response. With the apparent removal of an inhibitory sequence, the promoter-proximal 165-bp region also displayed a severalfold enhanced response to the combination of dexamethasone, IL-1, and IL-6. The sequence from -165 to -147, termed the A-element, was found to be crucial for all hormone regulatory functions. Two copies of the A-element linked to a heterologous promoter responded to the three hormones, but to a lesser degree than in the Hp gene promoter context. The regulatory elements of the rat Hp gene were similarly active in human hepatoma cells. Optimal regulation by IL-6 in HepG2 cells was, however, independent of the A-element. The A-element functioned in these cells exclusively as an IL-1 response sequence. The results suggest that genomic sequences upstream of the rat Hp gene suppress the regulation by specific cytokines more prominently in transient expression assays than in the normal chromosomal context. Moreover, the functional comparison indicated that specific regulatory regions of the rat Hp gene do not function identically in different hepatic cell types.

Regulated expression of a chimeric histone gene introduced into mouse fibroblasts

1985 ◽  
Vol 5 (9) ◽  
pp. 2316-2324
Author(s):  
R B Alterman ◽  
C Sprecher ◽  
R Graves ◽  
W F Marzluff ◽  
A I Skoultchi
Keyword(s):  
Histone Gene ◽  
Chimeric Gene ◽  
Regulatory Sequences ◽  
Mrna Levels ◽  
Histone Genes ◽  
Mouse Fibroblasts ◽  
Cis Acting ◽  
Regulated Expression ◽  
Chimeric Rna ◽  
The Stability

The regulated expression of a mouse histone gene was studied by DNA-mediated gene transfer. A chimeric H3 histone gene was constructed by fusing the 5' and 3' portions of two different mouse H3 histone genes. Transfection of the chimeric gene into mouse fibroblasts resulted in the production of chimeric mRNA at levels nearly equal to that of the total endogenous H3 histone mRNAs. Most chimeric RNA transcripts had correct 5' and 3' termini, and the chimeric mRNA was translated into an H3.1 protein that accumulated in the nucleus of the transfected cells. Expression of the chimeric gene was studied under several conditions in which the rate of transcription and the stability of endogenous H3 transcripts change. Chimeric mRNA levels were regulated in parallel with endogenous H3 mRNAs, suggesting that cis-acting regulatory sequences lie within or near individual histone genes. In addition to correctly initiated and terminated chimeric mRNA, we also detected a novel H3 transcript containing an additional 250 bases at the 3' end. Surprisingly, the longer transcript is polyadenylated and accumulates in the cytoplasm.

scholarly journals A combination of closely associated positive and negative cis-acting promoter elements regulates transcription of the skeletal alpha-actin gene.

1990 ◽  
Vol 10 (2) ◽  
pp. 528-538 ◽  
Author(s):  
K L Chow ◽  
R J Schwartz
Keyword(s):  
Transcriptional Activity ◽  
Primary Cultures ◽  
Gene Promoter ◽  
Regulatory Sequence ◽  
Actin Gene ◽  
Cell Type ◽  
Specific Expression ◽  
Cis Acting ◽  
Cell Type Specific Expression ◽  
Alpha Actin

The chicken skeletal alpha-actin gene promoter region provides at least a 75-fold-greater transcriptional activity in muscle cells than in fibroblasts. The cis-acting sequences required for cell type-restricted expression within this 200-base-pair (bp) region were elucidated by chloramphenicol acetyltransferase assays of site-directed Bg/II linker-scanning mutations transiently transfected into primary cultures. Four positive cis-acting elements were identified and are required for efficient transcriptional activity in myogenic cells. These elements, conserved across vertebrate evolution, include the ATAAAA box (-24 bp), paired CCAAT-box-associated repeats (CBARs; at -83 bp and -127 bp), and the upstream T+A-rich regulatory sequence (at -176 bp). Basal transcriptional activity in fibroblasts was not as dependent on the upstream CBAR or regions of the upstream T+A-rich regulatory sequence. Transfection experiments provided evidence that positive regulatory factors required for alpha-actin expression in fibroblasts are limiting. In addition, negative cis-acting elements were detected and found closely associated with the G+C-rich sequences that surround the paired CBARs. Negative elements may have a role in restricting developmentally timed expression in myoblasts and appear to inhibit promoter activity in nonmyogenic cells. Cell type-specific expression of the skeletal alpha-actin gene promoter is regulated by combinatorial and possibly competitive interactions between multiple positive and negative cis-acting elements.

scholarly journals Reconstitution of human Fc gamma RIII cell type specificity in transgenic mice.

1996 ◽  
Vol 183 (3) ◽  
pp. 1259-1263 ◽  
Author(s):  
M Li ◽  
U Wirthmueller ◽  
J V Ravetch
Keyword(s):  
Transgenic Mice ◽  
Nk Cells ◽  
Gene Promoter ◽  
Homologous Region ◽  
Cell Type ◽  
Cell Type Specificity ◽  
Specific Expression ◽  
Cis Acting ◽  
Sequence Elements ◽  
Flanking Sequences

The human low affinity receptors for the Fc domain of immunoglobulin G, Fc gamma RIII, are encoded by two genes (IIIA and IIIB) which share >95% sequence identity in both coding and flanking sequences. Despite this extraordinary sequence conservation, IIIA is expressed in natural killer (NK) cells and macrophages and is absent in neutrophils, whereas IIIB is expressed only in neutrophils. To determine the molecular basis for this differential expression, we have generated transgenic mice using the genomic sequences of IIIA and IIIB. IIIA and IIIB transgenic mice show faithful reconstitution of this human pattern of cell type specificity. To determine the cis acting sequence elements that confer this specificity, we constructed chimeric genes in which 5.8 kb of 5' sequences of the IIIB gene has been replaced with a homologous region from the IIIA gene, and conversely, IIIA 5' sequences have been substituted for the analogous region of the IIIB gene. Promoter swap transgenic mice that carry IIIA 5' flanking sequences express Fc gamma RIII in macrophages and NK cells. In contrast, promoter swap transgenic mice that contain IIIB 5' sequences express Fc gamma RIII in neutrophils only. These studies define the elements conferring the cell type-specific expression of the human Fc gamma RIII genes within the 5' flanking sequences and first intron of the human Fc gamma RIIIA and Fc gamma RIIIB genes.

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