A functional mutation in the AMPD1 promoter region affects promoter activity and breast meat freshness in chicken

2020 ◽  
Author(s):  
S. Yu ◽  
G. Wang ◽  
J. Liao ◽  
X. Chen
Keyword(s):  
Promoter Region ◽  
Promoter Activity ◽  
Breast Meat ◽  
Functional Mutation

The transcription factor E2F-1 mediates the autoregulation of RB gene expression

1994 ◽  
Vol 14 (1) ◽  
pp. 299-309
Author(s):  
B Shan ◽  
C Y Chang ◽  
D Jones ◽  
W H Lee
Keyword(s):  
Promoter Region ◽  
Promoter Activity ◽  
Cell Cycle Progression ◽  
Gene Mutations ◽  
Suppressor Gene ◽  
Recognition Sequence ◽  
Cycle Progression ◽  
Rb Gene ◽  
Transcription Factor E2f ◽  
Stimulation Of

The retinoblastoma (RB) gene is the prototype tumor suppressor gene. Mutations in this gene are often associated with the occurrence of various tumors. Several mutations have been found in the promoter region of the gene, suggesting that inappropriate transcriptional regulation of the RB gene contributes to tumorigenesis. Sequence analysis of the RB promoter has revealed a potential E2F recognition site within a region critical for RB gene transcription. By using the cloned E2F-1 gene, here we report that (i) RB expression is negatively regulated by its own gene product, (ii) E2F-1 binds specifically to an E2F recognition sequence in the RB promoter and transactivates the RB promoter, (iii) overexpression of RB suppresses E2F-1-mediated stimulation of RB promoter activity, and (iv) the expression of the RB gene is paralleled by the expression of the E2F-1 gene during cell cycle progression. These results demonstrate that expression of RB is negatively autoregulated through E2F-1.

Identification of functional TTF-1 and Sp1/Sp3 sites in the upstream promoter region of rabbit SP-B gene

2000 ◽  
Vol 278 (3) ◽  
pp. L477-L484 ◽  
Author(s):  
Ramgopal Margana ◽  
Kiflu Berhane ◽  
M. Nurul Alam ◽  
Vijayakumar Boggaram
Keyword(s):  
Promoter Region ◽  
Promoter Activity ◽  
Mutational Analysis ◽  
Surfactant Protein ◽  
Alveolar Type ◽  
Deletion Mapping ◽  
Clara Cells ◽  
Mobility Shift ◽  
Upstream Promoter ◽  
Upstream Promoter Region

Surfactant protein B (SP-B) is essential for the maintenance of biophysical properties and physiological function of pulmonary surfactant. SP-B mRNA is expressed in a cell type-restricted manner in alveolar type II and bronchiolar (Clara) epithelial cells of the lung and is developmentally induced. In NCI-H441 cells, a lung cell line with characteristics of Clara cells, a minimal promoter region comprising −236 to +39 nucleotides supports high-level expression of chloramphenicol acetyltransferase reporter activity. In the present investigation, we characterized the upstream promoter region, −236 to −140 nucleotides, that is essential for promoter activity. Deletion mapping identified two segments, −236 to −170 and −170 to −140 nucleotides, that are important for promoter activity. Mutational analysis and gel mobility shift experiments identified thyroid transcription factor-1, Sp1, and Sp3 as important trans-acting factors that bind to sequences in the upstream promoter region. Our data suggest that SP-B promoter activity is dependent on interactions between factors bound to upstream and downstream regions of the promoter.

Structural and functional characterization of the promoter region of the mouse c-Ki-ras gene

1987 ◽  
Vol 7 (7) ◽  
pp. 2592-2596
Author(s):  
E K Hoffman ◽  
S P Trusko ◽  
N Freeman ◽  
D L George
Keyword(s):  
Promoter Region ◽  
Promoter Activity ◽  
Functional Characterization ◽  
Genetic Material ◽  
Bidirectional Promoter ◽  
Adrenocortical Tumor ◽  
Ras Gene ◽  
Untranslated Exon ◽  
Size Heterogeneity

We isolated and characterized the 5' region of the mouse c-Ki-ras gene, including a 5' untranslated exon (exon 0). These studies used genetic material from Y1 mouse adrenocortical tumor cells in which the c-Ki-ras gene is amplified and overexpressed. Our data demonstrate that transcription initiates at multiple sites, predicting size heterogeneity at the 5' ends of the c-Ki-ras mRNAs. Using transient expression assays, we identified a genomic fragment within the 5' region which exhibits bidirectional promoter activity.

scholarly journals Coordinated High-Light Response of Genes Encoding Subunits of Photosystem I Is Achieved by AT-Rich Upstream Sequences in the Cyanobacterium Synechocystis sp. Strain PCC 6803

2007 ◽  
Vol 189 (7) ◽  
pp. 2750-2758 ◽  
Author(s):  
Masayuki Muramatsu ◽  
Yukako Hihara
Keyword(s):  
Photosystem I ◽  
Promoter Region ◽  
Promoter Activity ◽  
Light Response ◽  
High Light ◽  
Light Conditions ◽  
Low Light ◽  
Genes Encoding ◽  
Responsive Element ◽  
Pcc 6803

ABSTRACT Genes encoding subunits of photosystem I (PSI genes) in the cyanobacterium Synechocystis sp. strain PCC 6803 are actively transcribed under low-light conditions, whereas their transcription is coordinately and rapidly down-regulated upon the shift to high-light conditions. In order to identify the molecular mechanism of the coordinated high-light response, we searched for common light-responsive elements in the promoter region of PSI genes. First, the precise architecture of the psaD promoter was determined and compared with the previously identified structure of the psaAB promoter. One of two promoters of the psaAB genes (P1) and of the psaD gene (P2) possessed an AT-rich light-responsive element located just upstream of the basal promoter region. These sequences enhanced the basal promoter activity under low-light conditions, and their activity was transiently suppressed upon the shift to high-light conditions. Subsequent analysis of psaC, psaE, psaK1, and psaLI promoters revealed that their light response was also achieved by AT-rich sequences located at the −70 to −46 region. These results clearly show that AT-rich upstream elements are responsible for the coordinated high-light response of PSI genes dispersed throughout Synechocystis genome.

σBand SarA independently regulate polysaccharide intercellular adhesin production inStaphylococcus epidermidis

2007 ◽  
Vol 53 (1) ◽  
pp. 82-91 ◽  
Author(s):  
L D Handke ◽  
S R Slater ◽  
K M Conlon ◽  
Sinead T O'Donnell ◽  
M E Olson ◽  
...  
Keyword(s):  
Foreign Body ◽  
Staphylococcus Epidermidis ◽  
Promoter Region ◽  
Promoter Activity ◽  
Double Mutant ◽  
Direct Interaction ◽  
Transcriptional Analysis ◽  
Polysaccharide Intercellular Adhesin ◽  
Promoter Fusion ◽  
Biofilm Development

The production of polysaccharide intercellular adhesin (PIA) is an essential process in foreign body infections mediated by Staphylococcus epidermidis. Transcriptional regulation of the icaADBC operon, the genes responsible for production of enzymes that synthesize PIA, is multi-factorial and involves at least SarA and σB. Transcriptional and promoter fusion studies revealed that the decreased transcription of the icaADBC operon observed in a S. epidermidis 1457 sigB mutant is not mediated through a direct interaction of σB–RNA polymerase at the icaADBC promoter region but instead through the upregulation of IcaR, a known repressor of icaADBC transcription. Transcriptional analysis of a 1457 sigB–icaR double mutant confirmed that the decreased icaADBC transcript in 1457 sigB is IcaR dependent. Furthermore, primer extension studies suggest that the icaR promoter appears to be σAdependent, suggesting that σBindirectly controls icaR transcription through an unknown pathway. In addition, it was confirmed that the loss of SarA results in the loss of icaADBC transcription and PIA production in S. epidermidis. It was further demonstrated, through the over-production of SarA in 1457 sigB, that the loss of sarP1 promoter activity in 1457 sigB has little or no effect on the loss of PIA production in this mutant. Finally, it was demonstrated that PIA production could be restored in both 1457 sigB and 1457 sarA by complementing these mutants with a full-length icaADBC operon controlled by a cadmium-inducible noncognate promoter. It is concluded that σBand SarA operate independently of each other to regulate PIA production and biofilm development in S. epidermidis.Key words: Staphylococcus epidermidis, biofilm, σB, SarA, icaADBC.

scholarly journals Functional analysis of the promoter region of the human phosphotyrosine phosphatase activator gene: Yin Yang 1 is essential for core promoter activity

1999 ◽  
Vol 344 (3) ◽  
pp. 755-763 ◽  
Author(s):  
Veerle JANSSENS ◽  
Christine VAN HOOF ◽  
Ivo DE BAERE ◽  
Wilfried MERLEVEDE ◽  
Jozef GORIS
Keyword(s):  
Binding Sites ◽  
Promoter Region ◽  
Promoter Activity ◽  
Cpg Island ◽  
Luciferase Reporter ◽  
Binding Motif ◽  
Phosphotyrosine Phosphatase ◽  
Yin Yang 1 ◽  
Yin Yang

The phosphotyrosine phosphatase activator (PTPA) has been isolated as an in vitro regulator of protein phosphatase 2A. Human PTPA is encoded by a single gene, the structure and chromosomal localization of which have been determined in our previous work. Here we describe the further isolation, sequencing and functional characterization of the PTPA promoter region. In agreement with its ubiquitous expression, the PTPA promoter displays several characteristics of housekeeping genes: it lacks both a TATA-box and a CAAT-box, it is very GC-rich and it contains an unmethylated CpG island surrounding the transcription initiation site. Transient transfection experiments in different cell types with several truncated chimaeric luciferase reporter gene plasmids revealed the importance of the region between positions -67 and -39 for basal promoter activity. This region coincides remarkably well with the determined CpG island. Further analysis of this region demonstrated the presence of a Yin Yang 1 (YY1) binding motif at positions -52 to -44. Binding of YY1 to this sequence is demonstrated in bandshift and DNase I footprinting experiments. Another YY1 binding motif is found in the 5ʹ untranslated region, at positions +27 to +35. Mutations in either of these sites, abolishing YY1 binding in vitro, have differential effects on promoter activity. Point mutations in both sites completely abolish promoter activity. Moreover, induction of promoter activity by co-transfection with a YY1 expression plasmid is fully dependent upon the presence of both intact YY1 binding sites. Thus YY1 apparently mediates basal transcription of the human PTPA gene through two binding sites within its proximal promoter.

Downregulation of vasopressin V2 receptor promoter activity via V1a receptor pathway

2007 ◽  
Vol 292 (5) ◽  
pp. F1418-F1426 ◽  
Author(s):  
Yuichiro Izumi ◽  
Yushi Nakayama ◽  
Tomohiko Mori ◽  
Hiroki Miyazaki ◽  
Hideki Inoue ◽  
...  
Keyword(s):  
Promoter Region ◽  
Promoter Activity ◽  
Collecting Duct ◽  
V1a Receptor ◽  
Antidiuretic Effect ◽  
Collecting Ducts ◽  
V2 Receptor ◽  
Flanking Region ◽  
Pka Pathway

Vasopressin V1a and V2 receptors (V1aR and V2R, respectively) distribute in the collecting duct of the kidney. Although the function of V2R mediating the antidiuretic effect of AVP has been investigated in detail, the role of V1aR in the collecting ducts has not been elucidated. In the present study, we have investigated the role of the V1aR pathway in V2R promoter activity. We cloned the 5′-flanking region of rat V2R (rV2R) and investigated rV2R promoter activity in the LLC-PK1 cell line transfected to express rat V1aR (rV1aR) dominantly (LLC-PK1/rV1aR). AVP induced a transient increase, followed by a sustained decrease, of rV2R promoter activity in these cells. This AVP-induced decrease of rV2R promoter activity was inhibited by V1aR, but not V2R, antagonist. PMA mimicked this decrease of rV2R promoter activity. On the contrary, 8-(4-chlorophenylthio)-cAMP increased rV2R promoter activity. These PMA- and 8-(4-chlorophenylthio)-cAMP-induced effects were not observed on the deletion segment of the 5′-flanking region lacking CAAT and SP1 sites. In conclusion, 1) expression of the V2R is downregulated via the V1aR pathway in LLC-PK1/rV1aR cells, and 2) expression of the V2R is downregulated by the PMA-induced PKC pathway and upregulated by the cAMP-PKA pathway. These opposite effects of PKC and PKA appear to be regulated by the same promoter region of CAAT and SP1.

scholarly journals Ligand-dependent enhancement of human antithrombin gene expression by retinoid X receptor α and thyroid hormone receptor β

1996 ◽  
Vol 318 (1) ◽  
pp. 263-270 ◽  
Author(s):  
René W. L. M. NIESSEN ◽  
Farhad REZAEE ◽  
Pieter H. REITSMA ◽  
Marjolein PETERS ◽  
Jan J. M. de VIJLDER ◽  
...  
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Promoter Region ◽  
Promoter Activity ◽  
Thyroid Hormone Receptor ◽  
Retinoid X Receptor ◽  
Hepatoma Cell Line ◽  
Promoter Fragment ◽  
Thyroid Hormone Receptor Β

We studied potential modulators of antithrombin gene expression. A putative hormone response element (HRE) was identified by sequence similarity analysis of the antithrombin promoter, situated between nucleotides -92 and -54 relative to the transcription start site. This HRE contains three hexanucleotide motifs with an AGGTCA consensus, which are potential targets of members of the steroid/thyroid superfamily of nuclear receptors. Stimulation of the hepatoma cell line HepG2 with the receptor ligands l-3,5,3´-tri-iodothyronine, all-trans retinoic acid, or their combination, increased production of antithrombin into the culture medium by 1.3-, 1.6-, and 2.0-fold, respectively. In contrast, the receptor ligand 1,25-dihydroxycholecalciferol [1,25-(OH)2VitD3] did not influence antithrombin production. Analysis of promoter chloramphenicol acetyltransferase (CAT) constructs, showed that the first 86 bp of the antithrombin promoter region are sufficient for basal transcription. The DNA length polymorphism of 32 bp or 108 bp, located upstream of position -276, did not influence antithrombin promoter activity. The antithrombin promoter activity dropped to background values when deleting the region -97/-49 of promoter fragment -453/+57. Transactivation of the antithrombin promoter by retinoid X receptor α (RXRα) (5–7-fold) or thyroid hormone receptor β (TRβ) (4–5-fold) was only observed when at least -167/+57 bp of the promoter region is present in CAT constructs, and when the appropriate ligand of the nuclear receptor was added. This transactivation was not observed upon deletion of the antithrombin promoter region -97/-49. With three copies of the antithrombin promoter fragment -109/-42 in front of the thymidine kinase minimal promoter, transactivation was only obtained with RXRα, and not with TRβ. In conclusion, these results indicate that the ligand-dependent enhancement of antithrombin gene expression is regulated by RXRα as well as by TRβ. Transactivation of antithrombin gene expression by RXRα and TRβ appears to be dependent upon the presence of promoter region up to nucleotide -167. The HRE segment (-109/-42) only confers RXRα responsiveness to a heterologous promoter. Further study is needed to unravel the exact nature of this HRE and its 5´-flanking sequences.

scholarly journals The NRF-1/α-PAL transcription factor regulates human E2F6 promoter activity

2004 ◽  
Vol 383 (3) ◽  
pp. 529-536 ◽  
Author(s):  
Zoulika KHERROUCHE ◽  
Yvan DE LAUNOIT ◽  
Didier MONTE
Keyword(s):  
Promoter Region ◽  
Promoter Activity ◽  
Core Promoter ◽  
Dominant Negative ◽  
Site Directed Mutagenesis ◽  
Nuclear Respiratory Factor ◽  
Nuclear Respiratory Factor 1 ◽  
Dnase I Footprinting ◽  
Dominant Negative Form

E2F6 is widely expressed in human tissues and cell lines. Recent studies have demonstrated its involvement in developmental patterning and in the regulation of various genes implicated in chromatin remodelling. Despite a growing number of studies, nothing is really known concerning the E2F6 expression regulation. To understand how cells control E2F6 expression, we analysed the activity of the previously cloned promoter region of the human E2F6 gene. DNase I footprinting, gel electrophoreticmobility shift, transient transfection and site-directed mutagenesis experiments allowed the identification of two functional NRF-1/α-PAL (nuclear respiratory factor-1/α-palindrome-binding protein)-binding sites within the human E2F6 core promoter region, which are conserved in the mouse and rat E2F6 promoter region. Moreover, ChIP (chromatin immunoprecipitation) analysis demonstrated that overexpressed NRF-1/α-PAL is associated in vivo with the E2F6 promoter. Furthermore, overexpression of full-length NRF-1/α-PAL enhanced E2F6 promoter activity, whereas expression of its dominant-negative form reduced the promoter activity. Our results indicate that NRF-1/α-PAL is implicated in the regulation of basal E2F6 gene expression.

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