scholarly journals DNA-binding landscape of IRF3, IRF5 and IRF7 dimers: implications for dimer-specific gene regulation

2018 ◽  
Vol 46 (5) ◽  
pp. 2509-2520 ◽  
Author(s):  
Kellen K Andrilenas ◽  
Vijendra Ramlall ◽  
Jesse Kurland ◽  
Brandon Leung ◽  
Allen G Harbaugh ◽  
...  
2021 ◽  
Vol 49 (7) ◽  
pp. 3856-3875
Author(s):  
Marina Kulik ◽  
Melissa Bothe ◽  
Gözde Kibar ◽  
Alisa Fuchs ◽  
Stefanie Schöne ◽  
...  

Abstract The glucocorticoid (GR) and androgen (AR) receptors execute unique functions in vivo, yet have nearly identical DNA binding specificities. To identify mechanisms that facilitate functional diversification among these transcription factor paralogs, we studied them in an equivalent cellular context. Analysis of chromatin and sequence suggest that divergent binding, and corresponding gene regulation, are driven by different abilities of AR and GR to interact with relatively inaccessible chromatin. Divergent genomic binding patterns can also be the result of subtle differences in DNA binding preference between AR and GR. Furthermore, the sequence composition of large regions (>10 kb) surrounding selectively occupied binding sites differs significantly, indicating a role for the sequence environment in guiding AR and GR to distinct binding sites. The comparison of binding sites that are shared shows that the specificity paradox can also be resolved by differences in the events that occur downstream of receptor binding. Specifically, shared binding sites display receptor-specific enhancer activity, cofactor recruitment and changes in histone modifications. Genomic deletion of shared binding sites demonstrates their contribution to directing receptor-specific gene regulation. Together, these data suggest that differences in genomic occupancy as well as divergence in the events that occur downstream of receptor binding direct functional diversification among transcription factor paralogs.


2014 ◽  
Vol 30 (6) ◽  
pp. 211-219 ◽  
Author(s):  
Anne-Laure Todeschini ◽  
Adrien Georges ◽  
Reiner A. Veitia

2011 ◽  
Vol 13 (1) ◽  
pp. 95-102 ◽  
Author(s):  
Trevor Siggers ◽  
Abraham B Chang ◽  
Ana Teixeira ◽  
Daniel Wong ◽  
Kevin J Williams ◽  
...  

2001 ◽  
Vol 76 (1-5) ◽  
pp. 23-30 ◽  
Author(s):  
F. Claessens ◽  
G. Verrijdt ◽  
E. Schoenmakers ◽  
A. Haelens ◽  
B. Peeters ◽  
...  

Author(s):  
Marina Borschiwer ◽  
Melissa Bothe ◽  
Gözde Kibar ◽  
Alisa Fuchs ◽  
Stefanie Schöne ◽  
...  

AbstractThe glucocorticoid (GR) and androgen (AR) receptors execute unique functions in vivo, yet have nearly identical DNA binding specificities. To identify mechanisms that facilitate functional diversification among these transcription factor paralogs, we studied AR and GR in an equivalent cellular context. Analysis of chromatin and sequence features suggest that divergent binding, and corresponding gene regulation, are driven by different abilities of AR and GR to interact with relatively inaccessible chromatin. Divergent genomic binding patterns can also be the results of subtle differences in DNA binding preference between AR and GR. Furthermore, the sequence composition of large regions (>10 kb) surrounding selectively occupied binding sites differs significantly, indicating a role for the sequence environment in selectively guiding AR and GR to distinct binding sites. The comparison of binding sites that are shared between AR and GR shows that the specificity paradox can also be resolved by differences in the events that occur downstream of receptor binding. Specifically, we find that shared binding sites display receptor-specific enhancer activity, cofactor recruitment and changes in histone modifications. Genomic deletion of shared binding sites demonstrates their contribution to directing receptor-specific gene regulation. Together, these data suggest that differences in genomic occupancy as well as divergence in the events that occur downstream of receptor binding direct functional diversification among transcription factor paralogs.


2021 ◽  
Author(s):  
Isabel Regadas ◽  
Olle Dahlberg ◽  
Roshan Vaid ◽  
Oanh Ho ◽  
Sergey Belikov ◽  
...  

Cell ◽  
2021 ◽  
Author(s):  
Mineto Ota ◽  
Yasuo Nagafuchi ◽  
Hiroaki Hatano ◽  
Kazuyoshi Ishigaki ◽  
Chikashi Terao ◽  
...  

2011 ◽  
Vol 40 (8) ◽  
pp. 3524-3537 ◽  
Author(s):  
Ana I. Prieto ◽  
Christina Kahramanoglou ◽  
Ruhi M. Ali ◽  
Gillian M. Fraser ◽  
Aswin S. N. Seshasayee ◽  
...  

1992 ◽  
Vol 12 (8) ◽  
pp. 3614-3627
Author(s):  
P G Traber ◽  
G D Wu ◽  
W Wang

Sucrase-isomaltase (SI) is an enterocyte-specific gene which exhibits a complex pattern of expression during intestinal development and in the adult intestinal mucosa. In the studies described in this report, we demonstrate that enterocyte-specific transcription of the SI gene is regulated by an evolutionarily conserved promoter that extends approximately 180 bp upstream of the transcription start site. DNase I footprint analysis allowed the identification of three nuclear protein-binding sites within the SI promoter (SIF1, SIF2, and SIF3 [SI footprint]), each of which acted as a positive regulatory element for transcription in intestinal cell lines. SIF1 was shown to bind nuclear protein complexes present in primary mouse small intestinal cell and in an intestinal cell line (Caco-2). However, SIF1-binding proteins were absent in a variety of other epithelial and nonepithelial cells. In vitro mutagenesis experiments demonstrated that the SIF1 site is required for high-level promoter activity in intestinal cells. The SIF3 element formed prominent binding complexes with intestinal and liver nuclear extracts, whereas nuclear proteins from other epithelial and nonepithelial cells formed weaker complexes of different mobilities. The SIF2 element bound nuclear proteins in a pattern similar to that of SIF3, and cross-competition studies suggested that SIF2 and SIF3 may bind the same nuclear proteins. Taken together, these data have allowed the identification of novel DNA-binding proteins that play an important role in regulating intestine-specific transcription of the SI gene.


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