Cooperative Binding of the C.AhdI Controller Protein to the C/R Promoter and its Role in Endonuclease Gene Expression

2006 ◽  
Vol 358 (2) ◽  
pp. 523-531 ◽  
Author(s):  
J.E. McGeehan ◽  
I. Papapanagiotou ◽  
S.D. Streeter ◽  
G.G. Kneale
Keyword(s):  
Gene Expression ◽  
Cooperative Binding ◽  
Endonuclease Gene

scholarly journals Distinct mechanisms for regulation of the interleukin-8 gene involve synergism and cooperativity between C/EBP and NF-kappa B.

1993 ◽  
Vol 13 (11) ◽  
pp. 7191-7198 ◽  
Author(s):  
B Stein ◽  
A S Baldwin
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis Factor ◽  
Binding Site ◽  
Tumor Necrosis ◽  
Interleukin 8 ◽  
Cooperative Binding ◽  
Nf Kappa B ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

The interleukin-8 promoter is transcriptionally activated by interleukin-1, tumor necrosis factor alpha, phorbol myristate acetate, or hepatitis B virus X protein through a sequence located between positions -91 and -71. This region contains an NF-kappa B-like and a C/EBP-like binding site. We show here that several members of the NF-kappa B family, including p65, p50, p52, and c-Rel, can bind to this region, confirming an authentic NF-kappa B binding site in the interleukin-8 promoter. Further, C/EBP binds only weakly to the interleukin-8 promoter site. Electrophoretic mobility shift assays with proteins overexpressed in COS cells and with nuclear extracts from tumor necrosis factor alpha-stimulated HeLa cells demonstrated a strong cooperative binding of C/EBP to its site when NF-kappa B is bound to its adjacent binding site. Transfection studies lead to a model that suggests a highly complex regulation of interleukin-8 gene expression at multiple levels: independent binding of C/EBP and NF-kappa B to their respective sites, cooperative binding of C/EBP and NF-kappa B to DNA, and positive synergistic activation through the C/EBP binding site and inhibition through the NF-kappa B binding site by combinations of C/EBP and NF-kappa B. Thus, the ultimate regulation of interleukin-8 gene expression depends on the ratio of cellular C/EBP and NF-kappa B.

scholarly journals Distinct mechanisms for regulation of the interleukin-8 gene involve synergism and cooperativity between C/EBP and NF-kappa B

1993 ◽  
Vol 13 (11) ◽  
pp. 7191-7198 ◽  
Author(s):  
B Stein ◽  
A S Baldwin
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis Factor ◽  
Binding Site ◽  
Tumor Necrosis ◽  
Interleukin 8 ◽  
Cooperative Binding ◽  
Nf Kappa B ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

The interleukin-8 promoter is transcriptionally activated by interleukin-1, tumor necrosis factor alpha, phorbol myristate acetate, or hepatitis B virus X protein through a sequence located between positions -91 and -71. This region contains an NF-kappa B-like and a C/EBP-like binding site. We show here that several members of the NF-kappa B family, including p65, p50, p52, and c-Rel, can bind to this region, confirming an authentic NF-kappa B binding site in the interleukin-8 promoter. Further, C/EBP binds only weakly to the interleukin-8 promoter site. Electrophoretic mobility shift assays with proteins overexpressed in COS cells and with nuclear extracts from tumor necrosis factor alpha-stimulated HeLa cells demonstrated a strong cooperative binding of C/EBP to its site when NF-kappa B is bound to its adjacent binding site. Transfection studies lead to a model that suggests a highly complex regulation of interleukin-8 gene expression at multiple levels: independent binding of C/EBP and NF-kappa B to their respective sites, cooperative binding of C/EBP and NF-kappa B to DNA, and positive synergistic activation through the C/EBP binding site and inhibition through the NF-kappa B binding site by combinations of C/EBP and NF-kappa B. Thus, the ultimate regulation of interleukin-8 gene expression depends on the ratio of cellular C/EBP and NF-kappa B.

SV40 gene expression is modulated by the cooperative binding of T antigen to DNA

Cell ◽  
1981 ◽  
Vol 25 (2) ◽  
pp. 373-384 ◽  
Author(s):  
Richard M. Myers ◽  
Donald C. Rio ◽  
Alan K. Robbins ◽  
Robert Tjian
Keyword(s):  
Gene Expression ◽  
T Antigen ◽  
Cooperative Binding

scholarly journals Detection of cooperatively bound transcription factor pairs using ChIP-seq peak intensities and expectation maximization

2017 ◽  
Author(s):  
Vishaka Datta ◽  
Rahul Siddharthan ◽  
Sandeep Krishna
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Em Algorithm ◽  
Expectation Maximization ◽  
Cell Types ◽  
Eukaryotic Cells ◽  
Cooperative Binding ◽  
E Coli ◽  
Weak Binding ◽  
Better Than

AbstractTranscription factors (TFs) often work cooperatively, where the binding of one TF to DNA enhances the binding affinity of a second TF to a nearby location. Such cooperative binding is important for activating gene expression from promoters and enhancers in both prokaryotic and eukaryotic cells. Existing methods to detect cooperative binding of a TF pair rely on analyzing the sequence that is bound. We propose a method that uses, instead, only ChIP-seq peak intensities and an expectation maximization (CPI-EM) algorithm. We validate our method using ChIP-seq data from cells where one of a pair of TFs under consideration has been genetically knocked out. Our algorithm relies on our observation that cooperative TF-TF binding is correlated with weak binding of one of the TFs, which we demonstrate in a variety of cell types, including E. coli, S. cerevisiae and M. musculus cells. We show that this method performs significantly better than a predictor based only on the ChIP-seq peak distance of the TFs under consideration. This suggests that peak intensities contain information that can help detect the cooperative binding of a TF pair. CPI-EM also outperforms an existing sequence-based algorithm in detecting cooperative binding. The CPI-EM algorithm is available at https://github.com/vishakad/cpi-em.

scholarly journals Asymmetric Conservation within Pairs of Co-occurred Motifs Mediates Weak Direct Transcription Factor Binding in ChIP-seq Data

2020 ◽  
Author(s):  
Victor Levitsky ◽  
Dmitry Oshchepkov ◽  
Elena Zemlyanskaya ◽  
Tatyana Merkulova
Keyword(s):  
Gene Expression ◽  
Genomic Dna ◽  
Cooperative Binding ◽  
Substantial Portion ◽  
Single Chip ◽  
Conserved Motifs ◽  
Conserved Motif ◽  
Eukaryotic Gene Expression ◽  
Eukaryotic Gene ◽  
Ets Family

Background: Transcription factors (TFs) are main regulators of eukaryotic gene expression. The cooperative binding to genomic DNA of at least two TFs is the widespread mechanism of transcription regulation. Cooperating TFs can be revealed through the analysis of co-occurrence of their motifs. Methods: We applied Motifs Co-Occurrence Tool (MCOT) that predicted pairs of spaced or overlapped motifs (composite elements, CEs) for a single ChIP-seq dataset. We improved MCOT capability for prediction of asymmetric CEs with one of participating motifs possessing higher conservation than another does. Results: Analysis of 119 ChIP-seq datasets for 45 human TFs revealed that almost for all families of TFs the co-occurrence with an overlap between motifs of target TFs and more conserved partner motifs was significantly higher than that for less conserved partner motifs. The asymmetry toward partner TFs was the most clear for partner motifs of TFs from ETS family. Conclusion: Co-occurrence with an overlap of less conserved motif of a target TF and more conserved motifs of partner TFs explained a substantial portion of ChIP-seq data lacking conserved motifs of target TFs. Among other TF families, conservative motifs of TFs from ETS family were the most prone to mediate interaction of target TFs with its weak motifs in ChIP-seq.

scholarly journals A COOPERATIVE STOCHASTIC MODEL OF GENE EXPRESSION

2001 ◽  
Vol 12 (03) ◽  
pp. 413-420 ◽  
Author(s):  
SIDDHARTHA ROY ◽  
INDRANI BOSE ◽  
SUBHRANGSHU SEKHAR MANNA
Keyword(s):  
Gene Expression ◽  
Stochastic Model ◽  
Rna Polymerase ◽  
Single Cell ◽  
Large Fraction ◽  
Bimodal Distribution ◽  
Cooperative Binding

Recent experiments at the level of a single cell have shown that gene expression occurs in abrupt stochastic bursts. Further, in an ensemble of cells, the levels of proteins produced have a bimodal distribution. In a large fraction of cells, the gene expression is either off or has a high value. We propose a stochastic model of gene expression, the essential features of which are stochasticity and cooperative binding of RNA polymerase. The model can reproduce the bimodal behavior seen in experiments.

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