scholarly journals Izražanje transferinskih genov pri postrvih (Salmo sp.)

2018 ◽  
Vol 112 (1) ◽  
pp. 31
Author(s):  
Anja ČIBEJ ◽  
Simona SUŠNIK BAJEC
Keyword(s):  
Atlantic Salmon ◽  
Binding Sites ◽  
Promoter Region ◽  
Genomic Dna ◽  
Gene Promoter ◽  
Promoter Regions ◽  
Marble Trout ◽  
Potential Binding ◽  
Transferrin Gene ◽  
The Difference

Salmonidae family combines freshwater and anadromous fish species. Duplicates of numerous genomic DNA loci are characteristic for this family, some as a consequence of tetraploidisation, and others as independent doubling of discrete DNA regions. In the genus <em>Salmo</em>, duplication of transferrin gene in Atlantic salmon, brown and marble trout has been demonstrated. The aim of the study was to characterize the promoter region of both genes (TF1 and TF2) in all three species and to determine the ratio of expression of TF1 and TF2 in Atlantic salmon. Applying qPCR we showed that TF2 is expressed in Atlantic salmon six times weaker than TF1. It has been previously shown that the difference in the expression of both genes in brown and marble trout is even higher. The nucleotide sequence was determined for promoter regions of both genes in all species. In promoter region, microsatellite was found, which differs in length as well within species as between TF1 and TF2 locus, and four SNPs that differentiate TF1 and TF2. For Atlantic salmon, longer sequence of promoter region was determined. In TF1 gene, promoter contains a minisatellite, comprised of 37 bp long motif with over 20 replicates, while in TF2 minisatellite is not present. Analyzing potential binding sites in promoter region, functional elements for regulation of transferrin gene expression were found.

scholarly journals Induction of the Cellular E2F-1 Promoter by the Adenovirus E4-6/7 Protein

2000 ◽  
Vol 74 (5) ◽  
pp. 2084-2093 ◽  
Author(s):  
Joel Schaley ◽  
Robert J. O'Connor ◽  
Laura J. Taylor ◽  
Dafna Bar-Sagi ◽  
Patrick Hearing
Keyword(s):  
Dna Binding ◽  
Binding Site ◽  
Transient Expression ◽  
Binding Sites ◽  
Promoter Region ◽  
Fluorescent Protein ◽  
Protein Accumulation ◽  
Promoter Regions ◽  
Single Binding Site

ABSTRACT The adenovirus type 5 (Ad5) E4-6/7 protein interacts directly with different members of the E2F family and mediates the cooperative and stable binding of E2F to a unique pair of binding sites in the Ad5 E2a promoter region. This induction of E2F DNA binding activity strongly correlates with increased E2a transcription when analyzed using virus infection and transient expression assays. Here we show that while different adenovirus isolates express an E4-6/7 protein that is capable of induction of E2F dimerization and stable DNA binding to the Ad5 E2a promoter region, not all of these viruses carry the inverted E2F binding site targets in their E2a promoter regions. The Ad12 and Ad40 E2a promoter regions bind E2F via a single binding site. However, these promoters bind adenovirus-induced (dimerized) E2F very weakly. The Ad3 E2a promoter region binds E2F very poorly, even via a single binding site. A possible explanation of these results is that the Ad E4-6/7 protein evolved to induce cellular gene expression. Consistent with this notion, we show that infection with different adenovirus isolates induces the binding of E2F to an inverted configuration of binding sites present in the cellular E2F-1 promoter. Transient expression of the E4-6/7 protein alone in uninfected cells is sufficient to induce transactivation of the E2F-1 promoter linked to chloramphenicol acetyltransferase or green fluorescent protein reporter genes. Further, expression of the E4-6/7 protein in the context of adenovirus infection induces E2F-1 protein accumulation. Thus, the induction of E2F binding to the E2F-1 promoter by the E4-6/7 protein observed in vitro correlates with transactivation of E2F-1 promoter activity in vivo. These results suggest that adenovirus has evolved two distinct mechanisms to induce the expression of the E2F-1 gene. The E1A proteins displace repressors of E2F activity (the Rb family members) and thus relieve E2F-1 promoter repression; the E4-6/7 protein complements this function by stably recruiting active E2F to the E2F-1 promoter to transactivate expression.

scholarly journals SNP Diversity in CD14 Gene Promoter Suggests Adaptation Footprints in Trypanosome Tolerant N’Dama (Bos taurus) but not in Susceptible White Fulani (Bos indicus) Cattle

Genes ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 112 ◽  
Author(s):  
Olanrewaju B. Morenikeji ◽  
Anna L. Capria ◽  
Olusola Ojurongbe ◽  
Bolaji N. Thomas
Keyword(s):  
Genetic Diversity ◽  
Immune Response ◽  
Transcription Factor ◽  
Binding Sites ◽  
Promoter Region ◽  
Gene Promoter ◽  
Transcription Factor Binding Sites ◽  
Factor Binding ◽  
White Fulani ◽  
Cd14 Gene

Immune response to infections has been shown to be mediated by genetic diversity in pattern recognition receptors, leading to disease tolerance or susceptibility. We elucidated naturally occurring variations within the bovine CD14 gene promoter in trypanosome-tolerant (N’Dama) and susceptible (White Fulani) cattle, with genomic and computational approaches. Blood samples were collected from White Fulani and N’Dama cattle, genomic DNA extracted and the entire promoter region of the CD14 gene amplified by PCR. We sequenced this region and performed in silico computation to identify SNP variants, transcription factor binding sites, as well as micro RNAs in the region. CD14 promoter sequences were compared with the reference bovine genome from the Ensembl database to identify various SNPs. Furthermore, we validated three selected N’Dama specific SNPs using custom Taqman SNP genotyping assay for genetic diversity. In all, we identified a total of 54 and 41 SNPs at the CD14 promoter for N’Dama and White Fulani respectively, including 13 unique SNPs present in N’Dama only. The significantly higher SNP density at the CD14 gene promoter region in N’Dama may be responsible for disease tolerance, possibly an evolutionary adaptation. Our genotype analysis of the three loci selected for validation show that mutant alleles (A/A, C/C, and A/A) were adaptation profiles within disease tolerant N’Dama. A similar observation was made for our haplotype analysis revealing that haplotypes H1 (ACA) and H2 (ACG) were significant combinations within the population. The SNP effect prediction revealed 101 and 89 new transcription factor binding sites in N’Dama and White Fulani, respectively. We conclude that disease tolerant N’Dama possessing higher SNP density at the CD14 gene promoter and the preponderance of mutant alleles potentially confirms the significance of this promoter in immune response, which is lacking in susceptible White Fulani. We, therefore, recommend further in vitro and in vivo study of this observation in infected animals, as the next step for understanding genetic diversity relating to varying disease phenotypes in both breeds.

scholarly journals 8-OxoG in GC-rich Sp1 binding sites enhances gene transcription during adipose tissue development in juvenile mice

2019 ◽  
Author(s):  
Jong Woo Park ◽  
Young In Han ◽  
Tae Min Kim ◽  
Su Cheong Yeom ◽  
Jaeku Kang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Regulation ◽  
Adipose Tissue ◽  
Binding Sites ◽  
Gene Promoter ◽  
Tissue Development ◽  
Promoter Regions ◽  
Dna Lesion ◽  
Estrogen Response ◽  
Adipose Tissue Development

ABSTRACTThe oxidation of guanine to 8-oxoguanine (8-oxoG) is the most common type of oxidative DNA lesion. There is a growing body of evidence indicating that 8-oxoG is not only pre-mutagenic, but also plays an essential role in modulating gene expression along with its cognate repair proteins. In this study, we investigated the relationship between 8-oxoG formed under intrinsic oxidative stress conditions and gene expression in adipose and lung tissues of juvenile mice. We observed that transcriptional activity and the number of active genes were significantly correlated with the distribution of 8-oxoG in gene promoter regions, as determined by reverse-phase liquid chromatography/mass spectrometry (RP-LC/MS), and 8-oxoG and RNA sequencing. Gene regulation by 8-oxoG was not associated with the degree of 8-oxoG formation. Instead, genes with GC-rich transcription factor binding sites in their promoters became more active with increasing 8-oxoG abundance as also demonstrated by specificity protein 1 (Sp1)- and estrogen response element (ERE)-luciferase assays in human embryonic kidney (HEK293T) cells. These results indicate that the occurrence of 8-oxoG in GC-rich Sp1 binding sites is important for gene regulation during adipose tissue development.

scholarly journals 8-OxoG in GC-rich Sp1 binding sites enhances gene transcription in adipose tissue of juvenile mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jong Woo Park ◽  
Young In Han ◽  
Sung Woo Kim ◽  
Tae Min Kim ◽  
Su Cheong Yeom ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Regulation ◽  
Adipose Tissue ◽  
Binding Sites ◽  
Gene Promoter ◽  
Promoter Regions ◽  
Dna Lesion ◽  
Estrogen Response ◽  
Adipose Tissue Development ◽  
Specificity Protein

Abstract The oxidation of guanine to 8-oxoguanine (8-oxoG) is the most common type of oxidative DNA lesion. There is a growing body of evidence indicating that 8-oxoG is not only pre-mutagenic, but also plays an essential role in modulating gene expression along with its cognate repair proteins. In this study, we investigated the relationship between 8-oxoG formed under intrinsic oxidative stress conditions and gene expression in adipose and lung tissues of juvenile mice. We observed that transcriptional activity and the number of active genes were significantly correlated with the distribution of 8-oxoG in gene promoter regions, as determined by reverse-phase liquid chromatography/mass spectrometry (RP-LC/MS), and 8-oxoG and RNA sequencing. Gene regulation by 8-oxoG was not associated with the degree of 8-oxoG formation. Instead, genes with GC-rich transcription factor binding sites in their promoters became more active with increasing 8-oxoG abundance as also demonstrated by specificity protein 1 (Sp1)- and estrogen response element (ERE)-luciferase assays in human embryonic kidney (HEK293T) cells. These results indicate that the occurrence of 8-oxoG in GC-rich Sp1 binding sites is important for gene regulation during adipose tissue development.

Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 10045-10045
Author(s):  
Y. Ikawa ◽  
N. Sugimoto ◽  
S. Koizumi ◽  
A. Yachie ◽  
Y. Saikawa
Keyword(s):  
Binding Sites ◽  
Germ Line ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Gene Promoter ◽  
Epigenetic Mechanism ◽  
Gene Promoters ◽  
Promoter Regions ◽  
Cpg Dinucleotides ◽  
Pediatric Aml

10045 Background: Infant ALL displays distinct biologic and clinical features with a poor prognosis. The CD10-negative immunophenotype of infant ALL is a hallmark and provides a predictable signature of MLL rearrangements. While CD10 negativity reflects an earlier stage of B-cell development, complete IgH gene rearrangements (VDJH) show more mature IgH status. Discordance between immunophenotype and genotype of infant ALL suggests an aberrant process in immunophenotypic steps of differentiation or a secondary down-regulation of CD 10 expression associated with MLL rearrangements. We performed methylation analysis of full promoter regions of the CD10 gene to investigate epigenetic mechanisms responsible for CD10 negativity. Methods: CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germ-line MLL, CD10-positive pre-B ALL cell line, infant AML (M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJH status and methylation of CD10 gene promoters. Results: Three of 4 cases with infant ALL revealed complete rearrangements of VDJH gene with productive joints. Bisulfite sequencing of CD 10 type 1 and 2 promoters identified more than 84% of methylated CpG dinucleotides in all three CD10-negative infant ALL cases with MLL/AF4. The CpG dinucleotides distributed in the clusters of putative Sp 1 binding sites and functionally active regulatory regions of the promoters were fully methylated. In contrast, none or a few of the CpG dinucleotides were methylated in the CD10-positive ALL, AML (M5) with MLL/AF9 or AML (M2) with AML1/ETO. Conclusions: Structural evidence of dense methylation in the CD 10 gene promoter suggested that methylated transcription factor binding sites contribute to CD10 silencing as an epigenetic mechanism. [Table: see text] No significant financial relationships to disclose.

Molecular analysis of the differential hepatic expression of rat kininogen family genes

1993 ◽  
Vol 13 (11) ◽  
pp. 6766-6777
Author(s):  
H M Chen ◽  
W S Liao
Keyword(s):  
Binding Sites ◽  
Gene Promoter ◽  
Transcriptional Level ◽  
Evolutionary Divergence ◽  
Binding Affinities ◽  
Promoter Regions ◽  
Hepatic Expression ◽  
Basal Expression ◽  
Promoter Swapping ◽  
Hepatic Synthesis

Serum concentration of rat T1 kininogen increases 20- to 30-fold in response to acute inflammation, an induced hepatic synthesis regulated primarily at the transcriptional level. We have demonstrated by transient transfection analyses that rat T1 kininogen gene/chloramphenicol acetyltransferase (T1K/CAT) constructs are highly responsive to interleukin-6 and dexamethasone. In these studies we examined the regulation of a highly homologous K kininogen gene promoter and showed that it is minimally induced under identical conditions. The basal expression of the KK/CAT construct was, however, five- to sevenfold higher than that of the analogous T1K/CAT construct. Promoter-swapping experiments to examine the molecular basis of this differentially regulated basal expression showed that at least two K kininogen promoter regions are important for conferring its high basal expression: a distal 19-bp region (C box) constituted a binding site for C/EBP family proteins, and a proximal 66-bp region contained two adjacent binding sites for hepatocyte nuclear factor 3 (HNF-3). While the C box in the K kininogen promoter was able to interact with C/EBP transcription factors, the T1 kininogen promoter C box could not. In addition, HNF-3 binding sites of the K kininogen promoter demonstrated stronger affinities than those of the T1 kininogen promoter. Since C/EBP and HNF-3 are highly enriched in the liver and are known to enhance transcription of liver-specific genes, these differences in their binding activities thus accounted for the K kininogen gene's higher basal expression. Our studies demonstrated that evolutionary divergence of a few critical nucleotides may lead to subtle changes in the binding affinities of a transcription factor to its recognition site, profoundly altering expression of the downstream gene.

scholarly journals Characterization of a Mobile clpL Gene from Lactobacillus rhamnosus

2005 ◽  
Vol 71 (4) ◽  
pp. 2061-2069 ◽  
Author(s):  
Aki Suokko ◽  
Kirsi Savijoki ◽  
Erja Malinen ◽  
Airi Palva ◽  
Pekka Varmanen
Keyword(s):  
Elevated Temperature ◽  
Binding Sites ◽  
Inverted Repeat ◽  
Promoter Region ◽  
Lactobacillus Rhamnosus ◽  
Sequence Analyses ◽  
Promoter Regions ◽  
Repeat Structure ◽  
Genes Encoding

ABSTRACT Two genes encoding ClpL ATPase proteins were identified in a probiotic Lactobacillus rhamnosus strain, E-97800. Sequence analyses revealed that the genes, designated clpL1 and clpL2, share 80% identity. The clpL2 gene showed the highest degree of identity (98.5%) to a clpL gene from Lactobacillus plantarum WCFSI, while it was not detected in three other L. rhamnosus strains studied. According to Northern analyses, the expression of clpL1 and the clpL2 were induced during heat shock by >20- and 3-fold, respectively. The functional promoter regions were determined by primer extension analyses, and the clpL1 promoter was found to be overlapped by an inverted repeat structure identical to the conserved CIRCE element, indicating that clpL1 belongs to the HrcA regulon in L. rhamnosus. No consensus binding sites for HrcA or CtsR could be identified in the clpL2 promoter region. Interestingly, the clpL2 gene was found to be surrounded by truncated transposase genes and flanked by inverted repeat structures nearly identical to the terminal repeats of the ISLpl1 from L. plantarum HN38. Furthermore, clpL2 was shown to be mobilized during prolonged cultivation at elevated temperature. The presence of a gene almost identical to clpL2 in L. plantarum and its absence in other L. rhamnosus strains suggest that the L. rhamnosus E-97800 has acquired the clpL2 gene via horizontal transfer. No change in the stress tolerance of the ClpL2-deficient derivative of E-97800 compared to the parental strain was observed.

scholarly journals Nonparametric Tests for Differential Histone Enrichment with ChIP-Seq Data

2015 ◽  
Vol 14s1 ◽  
pp. CIN.S13972 ◽  
Author(s):  
Qian Wu ◽  
Kyoung-Jae Won ◽  
Hongzhe Li
Keyword(s):  
Gene Expression ◽  
Protein Interactions ◽  
Binding Sites ◽  
Negative Binomial ◽  
Kernel Smoothing ◽  
Gene Promoter ◽  
Nonparametric Tests ◽  
Promoter Regions ◽  
Experimental Conditions ◽  
Nonparametric Hypothesis Testing

Chromatin immunoprecipitation sequencing (ChIP-seq) is a powerful method for analyzing protein interactions with DNA. It can be applied to identify the binding sites of transcription factors (TFs) and genomic landscape of histone modification marks (HMs). Previous research has largely focused on developing peak-calling procedures to detect the binding sites for TFs. However, these procedures may fail when applied to ChIP-seq data of HMs, which have diffuse signals and multiple local peaks. In addition, it is important to identify genes with differential histone enrichment regions between two experimental conditions, such as different cellular states or different time points. Parametric methods based on Poisson/negative binomial distribution have been proposed to address this differential enrichment problem and most of these methods require biological replications. However, many ChIP-seq data usually have a few or even no replicates. We propose a nonparametric method to identify the genes with differential histone enrichment regions even without replicates. Our method is based on nonparametric hypothesis testing and kernel smoothing in order to capture the spatial differences in histone-enriched profiles. We demonstrate the method using ChIP-seq data on a comparative epigenomic profiling of adipogenesis of murine adipose stromal cells and the Encyclopedia of DNA Elements (ENCODE) ChIP-seq data. Our method identifies many genes with differential H3K27ac histone enrichment profiles at gene promoter regions between proliferating preadipocytes and mature adipocytes in murine 3T3-L1 cells. The test statistics also correlate with the gene expression changes well and are predictive to gene expression changes, indicating that the identified differentially enriched regions are indeed biologically meaningful.

Molecular organization of the human Raf-1 promoter region

1990 ◽  
Vol 10 (7) ◽  
pp. 3325-3333
Author(s):  
T W Beck ◽  
U Brennscheidt ◽  
G Sithanandam ◽  
J Cleveland ◽  
U R Rapp
Keyword(s):  
Promoter Region ◽  
Genomic Dna ◽  
Housekeeping Gene ◽  
Molecular Organization ◽  
Nucleotide Sequencing ◽  
Base Pairs ◽  
S1 Nuclease ◽  
Octamer Motif ◽  
Potential Binding ◽  
Potential Binding Site

A genomic DNA fragment containing the Raf-1 promoter region was isolated by using a cDNA extension clone. Nucleotide sequencing of genomic DNA clones, primer extension, and S1 nuclease assays have been used to identify the 5' ends of Raf-1 RNAs. Consistent with its ubiquitous expression, the Raf-1 promoter region had features of a housekeeping gene in that it was GC-rich (HTF-like), lacked TATA and CAAT boxes, and contained heterogeneous RNA start sites and four potential binding sites for the transcription factor SP1. In addition, an octamer motif (ATTTCAT), a potential binding site for the octamer family of transcription factors, was located at -734 base pairs. The Raf-1 promoter region drove reporter gene expression 30-fold over the promoterless reporter in Cos 7 cells.

scholarly journals Polymorphisms in the Promoter Region of Catalase Gene and Essential Hypertension

2005 ◽  
Vol 21 (1) ◽  
pp. 3-7 ◽  
Author(s):  
Xiao Feng Zhou ◽  
Jing Cui ◽  
Anita L. DeStefano ◽  
Irmarie Chazaro ◽  
Lindsay A. Farrer ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
African Americans ◽  
Promoter Region ◽  
Gene Promoter ◽  
Genetic Variations ◽  
Nucleotide Polymorphisms ◽  
Promoter Regions ◽  
Complex Disorders ◽  
Catalase Gene ◽  
Protein Properties

Genetic variations that predispose individuals to complex disorders, such as essential hypertension, may be found in gene coding regions, intronic regions or in gene promoter regions. Most studies have focused on gene variations that result in amino acid substitutions because they result in different isoforms of the protein, presumably resulting in differences in protein properties. Less attention has been placed on the role of intronic or promoter mutations. In this report, we examined two single nucleotide polymorphisms (SNPs) in the catalase (CAT) gene prompter region in a cohort of hypertensive Caucasians and African Americans with a Mass Spec based Homogenous MassEXTEND assay. We found an association when a specific combination of the two promoter SNPs was examined in Caucasians. No association was observed in African Americans. Our data suggest that genetic variations in the promoter region of catalase gene influence the susceptibility to essential hypertension. In addition, the genetic factors that contribute to hypertension maybe different between ethnic groups.

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