scholarly journals TF2LncRNA: Identifying Common Transcription Factors for a List of lncRNA Genes from ChIP-Seq Data

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Qinghua Jiang ◽  
Jixuan Wang ◽  
Yadong Wang ◽  
Rui Ma ◽  
Xiaoliang Wu ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Cell Line ◽  
Binding Sites ◽  
Regulatory Region ◽  
Specific Cell ◽  
Web Based ◽  
Genomic Technologies ◽  
Number Of Binding Sites ◽  
Transcription Regulators ◽  
On Chip

High-throughput genomic technologies like lncRNA microarray and RNA-Seq often generate a set of lncRNAs of interest, yet little is known about the transcriptional regulation of the set of lncRNA genes. Here, based on ChIP-Seq peak lists of transcription factors (TFs) from ENCODE and annotated human lncRNAs from GENCODE, we developed a web-based interface titled “TF2lncRNA,” where TF peaks from each ChIP-Seq experiment are crossed with the genomic coordinates of a set of input lncRNAs, to identify which TFs present a statistically significant number of binding sites (peaks) within the regulatory region of the input lncRNA genes. The input can be a set of coexpressed lncRNA genes or any other cluster of lncRNA genes. Users can thus infer which TFs are likely to be common transcription regulators of the set of lncRNAs. In addition, users can retrieve all lncRNAs potentially regulated by a specific TF in a specific cell line of interest or retrieve all TFs that have one or more binding sites in the regulatory region of a given lncRNA in the specific cell line. TF2LncRNA is an efficient and easy-to-use web-based tool.

scholarly journals TFEA.ChIP: a tool kit for transcription factor binding site enrichment analysis capitalizing on ChIP-seq datasets

2019 ◽  
Vol 35 (24) ◽  
pp. 5339-5340 ◽  
Author(s):  
Laura Puente-Santamaria ◽  
Wyeth W Wasserman ◽  
Luis del Peso
Keyword(s):  
Genomic Analysis ◽  
Enrichment Analysis ◽  
R Package ◽  
Supplementary Information ◽  
Web Based ◽  
Factor Binding Site ◽  
Gene Sets ◽  
Transcription Regulators ◽  
Computational Identification ◽  
On Chip

Abstract Summary The computational identification of the transcription factors (TFs) [more generally, transcription regulators, (TR)] responsible for the co-regulation of a specific set of genes is a common problem found in genomic analysis. Herein, we describe TFEA.ChIP, a tool that makes use of ChIP-seq datasets to estimate and visualize TR enrichment in gene lists representing transcriptional profiles. We validated TFEA.ChIP using a wide variety of gene sets representing signatures of genetic and chemical perturbations as input and found that the relevant TR was correctly identified in 126 of a total of 174 analyzed. Comparison with other TR enrichment tools demonstrates that TFEA.ChIP is an highly customizable package with an outstanding performance. Availability and implementation TFEA.ChIP is implemented as an R package available at Bioconductor https://www.bioconductor.org/packages/devel/bioc/html/TFEA.ChIP.html and github https://github.com/LauraPS1/TFEA.ChIP_downloads. A web-based GUI to the package is also available at https://www.iib.uam.es/TFEA.ChIP/ Supplementary information Supplementary data are available at Bioinformatics online.

scholarly journals Participation of Ets transcription factors in the glucocorticoid response of the rat tyrosine aminotransferase gene.

1994 ◽  
Vol 14 (6) ◽  
pp. 4116-4125 ◽  
Author(s):  
M L Espinás ◽  
J Roux ◽  
J Ghysdael ◽  
R Pictet ◽  
T Grange
Keyword(s):  
Transcription Factors ◽  
Binding Site ◽  
Cell Line ◽  
Binding Sites ◽  
Tyrosine Aminotransferase ◽  
Hierarchical Level ◽  
Detectable Effect ◽  
Independent Manner ◽  
Glucocorticoid Response

We have previously shown that two remote glucocorticoid-responsive units (GRUs) of the rat tyrosine aminotransferase (TAT) gene contain multiple binding sites for several transcription factor families, including the glucocorticoid receptor (GR). We report here the identification of two novel binding sites for members of the Ets family of transcription factors in one of these GRUs. One of these binding sites overlaps the major GR-binding site (GRBS), whereas the other is located in its vicinity. Inactivation of the latter binding site leads to a twofold reduction of the glucocorticoid response, whereas inactivation of the site overlapping the GRBS has no detectable effect. In vivo footprinting analysis reveals that the active site is occupied in a glucocorticoid-independent manner, in a TAT-expressing cell line, even though it is located at a position where there is a glucocorticoid-dependent alteration of the nucleosomal structure. This same site is not occupied in a cell line that does not express TAT but expresses Ets-related DNA-binding activities, suggesting the existence of an inhibitory effect of chromatin structure at a hierarchical level above the nucleosome. The inactive Ets-binding site that overlaps the GRBS is not occupied even in TAT-expressing cells. However, this same overlapping site can confer Ets-dependent stimulation of both basal and glucocorticoid-induced levels when it is isolated from the GRU and duplicated. Ets-1 expression in COS cells mimics the activity of the Ets-related activities present in hepatoma cells. These Ets-binding sites could participate in the integration of the glucocorticoid response of the TAT gene with signal transduction pathways triggered by other nonsteroidal extracellular stimuli.

scholarly journals Regulation of the yjjQ-bglJ Operon, Encoding LuxR-Type Transcription Factors, and the Divergent yjjP Gene by H-NS and LeuO

2007 ◽  
Vol 190 (3) ◽  
pp. 926-935 ◽  
Author(s):  
Thomas Stratmann ◽  
S. Madhusudan ◽  
Karin Schnetz
Keyword(s):  
Transcription Factors ◽  
Virulence Factor ◽  
Binding Sites ◽  
Regulatory Region ◽  
Gene Encoding ◽  
E Coli ◽  
Divergent Promoters ◽  
Nucleoprotein Complex ◽  
K 12 ◽  
Regulatory Sites

ABSTRACT The yjjQ and bglJ genes encode LuxR-type transcription factors conserved in several enterobacterial species. YjjQ is a potential virulence factor in avian pathogenic Escherichia coli. BglJ counteracts the silencing of the bgl (β-glucoside) operon by H-NS in E. coli K-12. Here we show that yjjQ and bglJ form an operon carried by E. coli K-12, whose expression is repressed by the histone-like nucleoid structuring (H-NS) protein. The LysR-type transcription factor LeuO counteracts this repression. Furthermore, the yjjP gene, encoding a membrane protein of unknown function and located upstream in divergent orientation to the yjjQ-bglJ operon, is likewise repressed by H-NS. Mapping of the promoters as well as the H-NS and LeuO binding sites within the 555-bp intergenic region revealed that H-NS binds to the center of the AT-rich regulatory region and distal to the divergent promoters. LeuO sites map to the center and to positions distal to the yjjQ promoters, while one LeuO binding site overlaps with the divergent yjjP promoter. This latter LeuO site is required for full derepression of the yjjQ promoters. The arrangement of regulatory sites suggests that LeuO restructures the nucleoprotein complex formed by H-NS. Furthermore, the data support the conclusion that LeuO, whose expression is likewise repressed by H-NS and which is a virulence factor in Salmonella enterica, is a master regulator that among other loci, also controls the yjjQ-bglJ operon and thus indirectly the presumptive targets of YjjQ and BglJ.

Deep Mining of Natural Genetic Variation in Erythroid Cells Reveals New Insights about In Vivo Transcription Factor Binding and Chromatin Accessibility

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 3879-3879
Author(s):  
Vivek Behera ◽  
Perry Evans ◽  
Carolyne J Face ◽  
Laavanya Sankaranarayanan ◽  
Gerd A. Blobel
Keyword(s):  
Transcription Factor ◽  
Genetic Variation ◽  
Transcription Factors ◽  
Cell Line ◽  
Cell Lines ◽  
Genetic Variants ◽  
Binding Sites ◽  
Chromatin Accessibility ◽  
Erythroid Cell

Abstract Erythroid transcription factors (TFs) control gene expression programs, lineage decisions, and disease outcomes. How transcription factors contact DNA has been studied extensively in vitro, but in vivo binding characteristics are less well understood as they are influenced in a reciprocal manner by chromatin accessibility and neighboring transcription factors. Here, we present a comparative analysis approach that takes advantage of non-coding sequence variation between functionally equivalent erythroid cell lines to conduct an in-depth analysis of erythroid TF binding profiles and chromatin features. Specifically, we analyzed ChIP-seq datasets to identify millions of genetic non-coding variants between the mouse erythroleukemia cell line (MEL), a GATA1-inducible erythroid progenitor cell line (G1E-ER4), and primary murine erythroblast cells. We found that while these cell lines are highly positively correlated in chromatin features, larger differences in TF binding intensity are correlated with higher degrees of genetic variation between cell lines. We next examined discriminatory genetic variants between the cell lines that are located in ChIP-seq peaks of the erythroid transcription factor GATA1. Hundreds of such variants fall within GATA1 motifs. Differential GATA1 binding intensities associated with the variants revealed nucleotide positions that contribute most to in vivo GATA1 chromatin occupancy and identified which alternative nucleotides are most likely to disrupt binding. Notably, this additional information about GATA1's in vivo nucleotide binding preferences improved prediction of GATA1 binding sites genome-wide. We applied similar approaches to determine the bp-resolution in vivo binding preferences of TAL1/SCL and CTCF. We additionally identified thousands of discriminatory genetic variants within GATA1 sites that fall outside canonical GATA elements but within binding sites of other known TFs. Association of these variants with differential GATA1 binding intensities revealed that the hematopoietic transcription factors TAL1/SCL and KLF1 positively regulate GATA1 chromatin occupancy. Strikingly, we identified a number of motifs not previously implicated in cooperating with GATA1 that positively impact GATA1 chromatin binding. Notably, we also defined motifs associated with negative regulation of GATA1 chromatin occupancy. Applying a similar analysis to TAL1/SCL and CTCF revealed additional motifs involved in regulating the chromatin occupancy of these TFs. Finally, we associated discriminatory genetic variation between erythroid cell lines with large changes in sub-kb-scale DNase hypersensitivity. We found that single base pair substitutions within or near a number of erythroid TF motifs, including that for the RUNX family of nuclear factors, are strongly associated with changes in chromatin accessibility. Our findings use novel methods in comparative ChIP-seq and DNase-seq analysis to reveal new insights about the genetic basis for erythroid TF chromatin occupancy and chromatin accessibility. Disclosures No relevant conflicts of interest to declare.

scholarly journals Global Egr1-miRNAs Binding Analysis in PMA-Induced K562 Cells Using ChIP-Seq

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Wei Wang ◽  
Dequang Zhou ◽  
Xiaolong Shi ◽  
Chao Tang ◽  
Xueying Xie ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Line ◽  
Cell Fate ◽  
Binding Sites ◽  
K562 Cells ◽  
Specific Cell ◽  
High Confidence ◽  
Erythroleukemia Cell ◽  
Pcr Assays ◽  
Microrna Genes

Although much is known about microRNAs' regulation in gene expression and their contributions in cell fate, to date, globally lineage-(cell-) specific identification of the binding events between a transcription factor and its targeting microRNA genes is still waiting for elucidation. In this paper, we performed a ChIP-Seq experiment to find the targeting microRNA genes of a transcription factor, Egr1, in human erythroleukemia cell line K562. We found Egr1 binding sites near the promoters of 124 distinct microRNA genes, accounting for about 42% of the miRNAs which have high-confidence predicted promoters (294). We also found EGR1 bind to another 63 pre-miRNAs. We chose 12 of the 187 microRNAs with Egr1 binding sites to perform ChIP-PCR assays and the positive binding signal from ChIP-PCR confirmed the ChIP-Seq results. Our experiments provide the first global binding profile between Egr1 and its targeting microRNA genes in PMA-treated K562 cells, which may facilitate the understanding of pathways controlling microRNA biology in this specific cell line.

scholarly journals MON-723 Identification of Thyrotrope Signature Genes and Regulatory Elements

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Alexandre Daly ◽  
Leonard Cheung ◽  
Michelle Brinkmeier ◽  
Sally Ann Camper
Keyword(s):  
Gene Expression ◽  
Risk Factors ◽  
Transcription Factors ◽  
Cell Line ◽  
Cell Lines ◽  
Binding Sites ◽  
Regulatory Elements ◽  
Genome Wide Association Studies ◽  
Expression Data ◽  
Enhancer Element

Abstract Recent genome wide association studies have begun to identify loci that are risk factors for sporadic pituitary adenomas, but the genes associated with these loci are unknown. In general, ~90% of GWAS hits are in noncoding regions, making it difficult to transition from genetic mapping to a biological understanding of risk factors. Recent studies that identify enhancer regions by undertaking large scale functional genomic annotation of non-coding elements like Encyclopedia of DNA Elements (ENCODE) have begun to yield a better understanding of some complex diseases. Dense molecular profiling maps of the transcriptome and epigenome have been generated for more than 250 cell lines and 150 tissues, but pituitary cell lines or tissues were not included. Epigenetic and gene expression data are emerging for somatotropes, gonadotropes and corticotropes, but there is very little available data on thyrotropes. We identified the transcription factors and epigenetic changes in chromatin that are associated with differentiation of POU1F1-expressing progenitors into thyrotropes using cell lines that represent an early, undifferentiated Pou1f1 lineage progenitor (GHF-T1) and a committed thyrotrope (TαT1). TαT1 is an excellent cell line for this purpose because it responds to TRH, retinoids, and secretes TSH in response to diurnal cues. We have also used genetic labeling and fluorescence activated cell sorting to purify thyrotropes from pituitaries of young mice and analyzed gene expression using single cell transcriptomics. We used the Assay for TransposaseAccessible Chromatin with sequencing (ATACseq) and Cleavage Under Target and Release Using Nuclease (CUT&RUN) to identify POU1F1 binding sites and histone marks associated with active enhancers, H3K27Ac and H3K4Me1, or inactive regions, H3K27Me3, in GHF-T1 and TαT1 cells. We integrated DNA accessibility, histone modification patterns, transcription factor binding and RNA expression data to identify regulatory elements and candidate transcriptional regulators. We identified POU1F1 binding sites that were unique to each cell line. For example, POU1F1 binds sites in and around Cga and Tshb only in TαT1 cells and Twist1 and Gli3 only in GHFT1 cells. POU1F1 binding sites are commonly associated with bZIP factor consensus binding sites in GHFT1 cells and Helix-Turn-Helix or basic Helix-Loop-Helix in TαT1 cells, suggesting classes of transcription factors that may recruit POU1F1 to unique sites. We validated enhancer function of novel elements we mapped near Tshb, Gata2, and Pitx1 by transfection in TαT1 cells. Finally, we confirmed that an enhancer element near Tshb can drive expression in thyrotropes of transgenic mice. These data extend the ENCODE analysis to an organ that is critical for growth and metabolism. This information could be valuable for understanding pituitary development and disease pathogenesis.

Participation of Ets transcription factors in the glucocorticoid response of the rat tyrosine aminotransferase gene

1994 ◽  
Vol 14 (6) ◽  
pp. 4116-4125
Author(s):  
M L Espinás ◽  
J Roux ◽  
J Ghysdael ◽  
R Pictet ◽  
T Grange
Keyword(s):  
Transcription Factors ◽  
Binding Site ◽  
Cell Line ◽  
Binding Sites ◽  
Tyrosine Aminotransferase ◽  
Hierarchical Level ◽  
Detectable Effect ◽  
Independent Manner ◽  
Glucocorticoid Response

We have previously shown that two remote glucocorticoid-responsive units (GRUs) of the rat tyrosine aminotransferase (TAT) gene contain multiple binding sites for several transcription factor families, including the glucocorticoid receptor (GR). We report here the identification of two novel binding sites for members of the Ets family of transcription factors in one of these GRUs. One of these binding sites overlaps the major GR-binding site (GRBS), whereas the other is located in its vicinity. Inactivation of the latter binding site leads to a twofold reduction of the glucocorticoid response, whereas inactivation of the site overlapping the GRBS has no detectable effect. In vivo footprinting analysis reveals that the active site is occupied in a glucocorticoid-independent manner, in a TAT-expressing cell line, even though it is located at a position where there is a glucocorticoid-dependent alteration of the nucleosomal structure. This same site is not occupied in a cell line that does not express TAT but expresses Ets-related DNA-binding activities, suggesting the existence of an inhibitory effect of chromatin structure at a hierarchical level above the nucleosome. The inactive Ets-binding site that overlaps the GRBS is not occupied even in TAT-expressing cells. However, this same overlapping site can confer Ets-dependent stimulation of both basal and glucocorticoid-induced levels when it is isolated from the GRU and duplicated. Ets-1 expression in COS cells mimics the activity of the Ets-related activities present in hepatoma cells. These Ets-binding sites could participate in the integration of the glucocorticoid response of the TAT gene with signal transduction pathways triggered by other nonsteroidal extracellular stimuli.

scholarly journals The Latency-Associated Nuclear Antigen Encoded by Kaposi's Sarcoma-Associated Herpesvirus Activates Two Major Essential Epstein-Barr Virus Latent Promoters

2001 ◽  
Vol 75 (19) ◽  
pp. 9446-9457 ◽  
Author(s):  
Angela K. Groves ◽  
Murray A. Cotter ◽  
Chitra Subramanian ◽  
Erle S. Robertson
Keyword(s):  
Transcription Factors ◽  
Cell Line ◽  
Binding Sites ◽  
Kaposi's Sarcoma ◽  
Epstein Barr Virus ◽  
Kaposi’S Sarcoma ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Epstein Barr ◽  
Kaposi’S Sarcoma Associated Herpesvirus

ABSTRACT The latency-associated nuclear antigen (LANA) encoded by the Kaposi's sarcoma-associated herpesvirus (KSHV) is expressed in the majority of KSHV-infected cells and in cells coinfected with Epstein-Barr virus (EBV). In coinfected body cavity-based lymphomas (BCBLs), EBV latent membrane protein 1 (LMP1), which is essential for B-lymphocyte transformation, is expressed. EBNA2 upregulates the expression of LMP1 and other cellular genes through specific interactions with cellular transcription factors tethering EBNA2 to its responsive promoters. In coinfected BCBL cells, EBNA2 is not detected but LANA, which is constitutively expressed, contains motifs suggestive of potential transcriptional activity. Additionally, recent studies have shown that LANA is capable of activating cellular promoters. Therefore, we investigated whether LANA can affect transcription from two major EBV latent promoters. In this study, we demonstrated that LANA can efficiently transactivate both the LMP1 and C promoters in the human B-cell line BJAB as well as in the human embryonic kidney 293 cell line. Moreover, we demonstrated that specific domains of LANA containing the putative leucine zipper and the glutamic acid-rich region are highly effective in upregulating these viral promoters, while the amino-terminal region (435 amino acids) exhibited little or no transactivation activity in our assays. We also specifically tested truncations of the LMP1 promoter element and showed that the −204 to +40 region had increased levels of activation compared with a larger region, −512 to +40, which contains two recombination signal-binding protein Jκ binding sites. The smaller, −204 to +40 promoter region contains specific binding sites for the Ets family transcription factor PU.1, transcription activating factor/cyclic AMP response element, and Sp1, all of which are known to function as activators of transcription. Our data therefore suggest a potential role for LANA in regulation of the major EBV latent promoters in KSHV- and EBV-coinfected cells. Furthermore, LANA may be able to activate transcription of viral and cellular promoters in the absence of EBNA2, potentially through association with transcription factors bound to their cognate sequences within the −204 to +40 region. This regulation of viral gene expression is critical for persistence of these DNA tumor viruses and most likely involved in mediating the oncogenic process in these coinfected cells.

scholarly journals Promoter elements in Drosophila melanogaster revealed by sequence analysis.

Genetics ◽  
1995 ◽  
Vol 139 (3) ◽  
pp. 1359-1369 ◽  
Author(s):  
I R Arkhipova
Keyword(s):  
Drosophila Melanogaster ◽  
Transcription Factors ◽  
Binding Sites ◽  
Promoter Region ◽  
Gc Content ◽  
Proximal Promoter ◽  
Start Site ◽  
Sequence Organization ◽  
Number Of Binding Sites ◽  
Multiple Sequences

Abstract A Drosophila Promoter Database containing 252 independent Drosophila melanogaster promoter entries has been compiled. The database and its subsets have been searched for overrepresented sequences. The analysis reveals that the proximal promoter region displays the most dramatic nucleotide sequence irregularities and exhibits a tripartite structure, consisting of TATA at -25/-30 bp, initiator (Inr) at +/- 5 bp and a novel class of downstream elements at +20/+30 bp from the RNA start site. These latter elements are also strand-specific. However, they differ from TATA and Inr in several aspects: (1) they are represented not by a single, but by multiple sequences, (2) they are shorter, (3) their position is less strictly fixed with respect to the RNA start site, (4) they emerge as a characteristic feature of Drosophila promoters and (5) some of them are strongly overrepresented in the TATA-less, but not TATA-containing, subset. About one-half of known Drosophila promoters can be classified as TATA-less. The overall sequence organization of the promoter region is characterized by an extended region with an increase in GC-content and a decrease in A, which contains a number of binding sites for Drosophila transcription factors.

Translocation of transcription regulators into the nucleus during granulocyte commitment of HL-60 cells

2003 ◽  
Vol 81 (4) ◽  
pp. 285-295 ◽  
Author(s):  
Ruta Navakauskiene ◽  
Agné Kulyte ◽  
Grazina Treigyte ◽  
Arunas Gineitis ◽  
Karl-Eric Magnusson
Keyword(s):  
Transcription Factors ◽  
Retinoic Acid ◽  
Cell Line ◽  
Protein Level ◽  
Lineage Commitment ◽  
Granulocytic Differentiation ◽  
Nuclear Level ◽  
Differentiated Cells ◽  
Pathway Expression ◽  
Transcription Regulators

Expression of transcription factors required for lineage commitment of differentiating cells (C/EBPβ and c-Myb) and for survival of differentiated cells (STATs and NFκB) was examined in the HL-60 cell line. Differentiation was induced by treating the cells with retinoic acid. c-Myb expression in the nucleus restored at the precommitment stage (18 h) what concurred with the highest nuclear level of C/EBPβ, which suggests a combinatorial interaction of these transcription factors in the granulocytic signalling pathway. Expression of STAT5a and STAT5b varied during differentiation, whereas no significant changes were seen in STAT3 levels. Increased cytosolic level of NFκB p65 during precommitment and commitment stages of granulocytic differentiation coincided with augmentation of the STAT5a protein level, which could be evidence of their possible cooperation during granulocytic-lineage commitment of HL-60 cells. Our results suggest that the studied transcription factors cooperatively promote signalling in the differentiating promyelocytic HL-60 cell line in response to retinoic acid.Key words: C/EBP, Myb, STAT, NFκB, phosphorylation.

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