scholarly journals In vivo footprinting reveals unique cis-elements and different modes of hypoxic induction in maize Adh1 and Adh2.

1991 ◽  
Vol 3 (2) ◽  
pp. 159-168 ◽  
Author(s):  
A L Paul ◽  
R J Ferl
Keyword(s):  
Cis Elements ◽  
Hypoxic Induction ◽  
In Vivo Footprinting

scholarly journals A highly sensitive in vivo footprinting technique for condition-dependent identification of cis elements

2013 ◽  
Vol 42 (1) ◽  
pp. e1-e1 ◽  
Author(s):  
Rita Gorsche ◽  
Birgit Jovanovic ◽  
Loreta Gudynaite-Savitch ◽  
Robert L. Mach ◽  
Astrid R. Mach-Aigner
Keyword(s):  
Cis Elements ◽  
Highly Sensitive ◽  
In Vivo Footprinting

scholarly journals Multiple single-stranded cis elements are associated with activated chromatin of the human c-myc gene in vivo.

1996 ◽  
Vol 16 (6) ◽  
pp. 2656-2669 ◽  
Author(s):  
G A Michelotti ◽  
E F Michelotti ◽  
A Pullner ◽  
R C Duncan ◽  
D Eick ◽  
...  
Keyword(s):  
Binding Protein ◽  
Single Strand ◽  
Upstream Sequence ◽  
Cis Elements ◽  
Sequence Element ◽  
S1 Nuclease ◽  
Heterogeneous Nuclear Ribonucleoprotein ◽  
Myc Gene ◽  
Nuclear Ribonucleoprotein

Transcription activation and repression of eukaryotic genes are associated with conformational and topological changes of the DNA and chromatin, altering the spectrum of proteins associated with an active gene. Segments of the human c-myc gene possessing non-B structure in vivo located with enzymatic and chemical probes. Sites hypertensive to cleavage with single-strand-specific S1 nuclease or the single-strand-selective agent potassium permanganate included the major promoters P1 and P2 as well as the far upstream sequence element (FUSE) and CT elements, which bind, respectively, the single-strand-specific factors FUSE-binding protein and heterogeneous nuclear ribonucleoprotein K in vitro. Active and inactive c-myc genes yielded different patterns of S1 nuclease and permanganate sensitivity, indicating alternative chromatin configurations of active and silent genes. The melting of specific cis elements of active c-myc genes in vivo suggested that transcriptionally associated torsional strain might assist strand separation and facilitate factor binding. Therefore, the interaction of FUSE-binding protein and heterogeneous nuclear ribonucleoprotein K with supercoiled DNA was studied. Remarkably, both proteins recognize their respective elements torsionally strained but not as liner duplexes. Single-strand- or supercoil-dependent gene regulatory proteins may directly link alterations in DNA conformation and topology with changes in gene expression.

In Vivo Footprinting of the Interaction of Proteins with DNA and RNA

1997 ◽  
pp. 73-109 ◽  
Author(s):  
Thierry Grange ◽  
Gildas Rigaud ◽  
Edouard Bertrand ◽  
Micheline Fromont-Racine ◽  
Maria Lluisa Espinás ◽  
...  
Keyword(s):  
Dna And Rna ◽  
In Vivo Footprinting

Cytokine-induced changes in chromatin structure and in vivo footprints in the inducible NOS promoter

2001 ◽  
Vol 280 (3) ◽  
pp. L390-L399 ◽  
Author(s):  
Jane K. Mellott ◽  
Harry S. Nick ◽  
Michael F. Waters ◽  
Timothy R. Billiar ◽  
David A. Geller ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protein Interactions ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Specific Pattern ◽  
Mrna Levels ◽  
Inos Gene ◽  
In Vivo Footprinting ◽  
Induced Changes

Transcription of the human inducible nitric oxide synthase ( iNOS) gene is regulated by inflammatory cytokines in a tissue-specific manner. To determine whether differences in cytokine-induced mRNA levels between pulmonary epithelial cells (A549) and hepatic biliary epithelial cells (AKN-1) result from different protein or DNA regulatory mechanisms, we identified cytokine-induced changes in DNase I-hypersensitive (HS) sites in 13 kb of the iNOS 5′-flanking region. Data showed both constitutive and inducible HS sites in an overlapping yet cell type-specific pattern. Using in vivo footprinting and ligation-mediated PCR to detect potential DNA or protein interactions, we examined one promoter region near −5 kb containing both constitutive and cytokine-induced HS sites. In both cell types, three in vivo footprints were present in both control and cytokine-treated cells, and each mapped within a constitutive HS site. The remaining footprint appeared only in response to cytokine treatment and mapped to an inducible HS site. These studies, performed on chromatin in situ, identify a portion of the molecular mechanisms regulating transcription of the human iNOS gene in both lung- and liver-derived epithelial cells.

Genomic sequencing and in vivo footprinting

1989 ◽  
Vol 176 (2) ◽  
pp. 201-208 ◽  
Author(s):  
H.P. Saluz ◽  
J.P. Jost
Keyword(s):  
Genomic Sequencing ◽  
In Vivo Footprinting

Lineage-Specific Transcriptional Regulation of GATA1 Is Dependent on Lineage-Specific Utilisation of Multiple Cis-Elements and Haematopoietic Transcription Factors.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1610-1610
Author(s):  
Paresh Vyas ◽  
Boris Guyot ◽  
Veronica Valverde-Garduno ◽  
Eduardo Anguita ◽  
Isla Hamlett ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Dnase I ◽  
Red Cells ◽  
Erythroid Cells ◽  
Cis Elements ◽  
Dnase I Hypersensitive Sites ◽  
Hypersensitive Sites ◽  
Transcription Factor Occupancy

Abstract Normal differentiation of red cells, platelets and eosinophils from a myeloid progenitor requires expression of the transcription factor GATA1. Moreover, GATA1 expression level influences lineage output; higher levels promote erythromegakaryocytic differentiation and lower levels eosinophil maturation. Conversely, repression of GATA1 expression is required for monocyte/neutrophil development. GATA1 expression is principally controlled transcriptionally. Thus, dissecting the molecular basis of transcriptional control of GATA1 expression will be one important facet in understanding how myeloid lineages are specified. To address this question we sought to identify all DNA sequences important for GATA1 expression. Previous analysis identified 3 murine (m)Gata1 cis-elements (an upstream enhancer, mHS-3.5, a haematopoietic IE promoter and elements in a GATA1 intron, mHS+3.5) conserved in sequence between human(h) and mouse. These studies also suggested additional unidentified elements were required for erythroid and eosinophil GATA1 expression. We compared sequence, mapped DNase I hypersensitive sites (HS) and determined histone H3/H4 acetylation over ~120 kb flanking the hGATA1 locus and corresponding region in mouse to pinpoint cis-elements. Remarkably, despite lying in a ~10 MB conserved syntenic segment, the chromatin structures of both GATA1 loci are strikingly different. Two previously unidentified haematopoietic cis-elements, one in each species (mHS-25 and hHS+14), are not conserved in position and sequence and have enhancer activity in erythroid cells. Chromatin immunoprecipitation studies show both mHS-25 and hHS+14 are bound in vivo in red cells by the transcription factors GATA1, SCL, LMO2, Ldb1. These findings suggest that some cis-elements regulating human and mouse GATA1 genes differ. Further analysis of in vivo transcription factor occupancy at GATA1 cis-elements in primary mouse eosinophils and red cells, megakaryocytic cells (L8057) and control fibroblasts show lineage- and cis-element-specific patterns of regulator binding (see table below). In red cells and megakaryocytes, GATA1, SCL, LMO2 and Ldb1 bind at two regulatory elements (mhHS-25 and mHS-3.5). Interestingly, the megakaryocyte transcriptional regulator Fli1 factor binds to mHS+3.5 specifically in megakaryocytes. In eosinophils, a different pattern of DNase I HS and transcription factor binding is seen. GATA1, PU.1 and C/EBPe (all regulate eosinophil gene expression) bind IE promoter and/or mHS+3.5. Collectively, these results suggest lineage-specific GATA1 expession is dependent on combinations of cis-elements and haematopoietic trans-acting factors that are unique for each lineage. DNase I Hypersensitive sites and transcription factor occupancy at mGATA1 cis-elements. mHS-26/-25* mHS-3.5 mIE mHS+3.5 m: mouse, h: human, *: HS identified in this study, TF: transcription factor Primary erythroid cells HS present, GATA1, SCL, LMO2, Ldb1 HS present, GATA1, SCL, LMO2, Ldb1 HS present, GATA1 HS present, GATA1 Megakaryocytic cells HS present, GATA1, SCL, LMO2, Ldb1 HS present, GATA1, SCL, LMO2, Ldb1 HS present, GATA1 HS present, GATA1 and Fli1 Primary eosinophils HS absent HS present, No TF detected HS present, GATA1 and C/EBPε HS present, GATA1, C/EBP ε and PU.1 Fibroblasts HS absent HS absent HS absent HS absent

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