UV Light as a Footprinting Agent: Modulation of UV-induced DNA Damage by Transcription Factors Bound at the Promoters of Three Human Genes

Tornaletti, Silvia; Pfeifer, Gerd P.

doi:10.1006/jmbi.1995.0331

Cited by 125 publications

(102 citation statements)

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“…All the mutational hot spots (codon 175, 245, 248, 273, 282) contain CpG dinucleotide and the cytosine of this dinucleotide is often methylated in mammalian cells (Tornaletti and Pfeifer, 1995b;Soussi and Beroud, 2003). Both exogenous carcinogens (for example UV) and endogenous mutagens (such as altered cell metabolism) can target methylated CpG dinucleotide, leading to a high rate of transitions in p53 (Tornaletti and Pfeifer, 1995a;Denissenko et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Maximum likelihood analysis of mammalian p53 indicates the presence of positively selected sites and higher tumorigenic mutations in purifying sites

Khan

Rydén²,

Chowdhury

et al. 2011

Gene

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Section: Discussionmentioning

confidence: 99%

Maximum likelihood analysis of mammalian p53 indicates the presence of positively selected sites and higher tumorigenic mutations in purifying sites

Khan

Rydén²,

Chowdhury

et al. 2011

Gene

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“…Ultraviolet light induces the formation of pyrimidine dimers that can be subsequently converted into double strand DNA breaks. Studies on the PKG1, JUN, PCNA, and FOS gene promoters have demonstrated suppression or enhancement of UV photoproduct formation associated specifically with known sites of in vivo protein/DNA interaction (34,35). Analysis of CIITA promoter III demonstrates two strong photoproduct enhancements on the lower DNA strand at the ARE-1 element (Fig.…”

Section: In Vivo Genomic Footprinting Analysis In B-lymphocytes Detecmentioning

confidence: 97%

A Novel Element and a TEF-2-like Element Activate the Major Histocompatibility Complex Class II Transactivator in B-lymphocytes

Ghosh

Piskurich

Wright

et al. 1999

Journal of Biological Chemistry

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Major histocompatibility complex (MHC) class II molecules play a central role in immune responses, and transcription of this family of genes requires the MHC class II transactivator (CIITA). CIITA has four promoters, which are transcribed in a tissue-specific manner. CIITA promoter III is constitutively active in mature B-lymphocytes. This report now describes the minimal 319-base pair promoter region necessary for maximal transcriptional activity in B-lymphocytes. Ultraviolet light and dimethylsulfate in vivo genomic footprinting analyses reveal five occupied DNA sequence elements present in intact B-lymphocytes. Functional analysis of these elements using promoter deletions and site-specific mutations demonstrates that at least two of the sites occupied in vivo are critical for transcriptional activity. In vitro protein/DNA analysis suggests that one of the sites is a TEF-2-like element and the other is occupied by a novel transcription activator. In addition, nuclear factor-1 associates with the promoter both in vivo and in vitro. In myeloma cell lines, loss of CIITA transcription correlates with a completely unoccupied CIITA promoter III. These findings suggest that CIITA transcription in B-lymphocytes is activated through at least two strong promoter elements, while loss of expression in myeloma cells is mediated through changes in promoter assembly.Major histocompatibility complex (MHC) 1 class II molecules play a fundamental role in presenting exogenous antigenic peptides to CD4 ϩ helper T lymphocytes (1). These activated CD4 ϩ T cells release stimulatory cytokines that augment the response of CD8 ϩ cytotoxic T lymphocytes (2). Constitutive expression of MHC class II molecules is restricted to professional antigen-presenting cells, such as B lymphocytes and dendritic cells, and can be induced by interferon-␥ (IFN-␥) in macrophages, endothelial cells, and fibroblasts (3, 4). The MHC class II family of genes are coordinately regulated at the level of transcription through a conserved trimeric promoter motif (3, 5). A major component of this transcription complex was cloned by genetic complementation of an in vitro mutagenized MHC class II negative B cell line, RJ2.2.5. This component was named the MHC class II transactivator (CIITA) and restored MHC class II cell surface expression in one subgroup of bare lymphocyte syndrome patient cells (6). CIITA has since been shown to be a key regulatory molecule in the expression of all the known genes involved in the MHC class II antigen-presenting pathway (6 -9). CIITA is required for constitutive expression of MHC class II on B-lymphocytes (10) and with a few exceptions, such as in respiratory epithelial cells and dendritic cells (11,12), is required for cytokine-induced expression in other cell types. Mice in which functional CIITA protein was ablated clearly demonstrated an absolute requirement for CI-ITA in B cell expression of MHC class II (13). It has been shown that the CIITA gene has four distinct promoters each transcribing a unique first exon, which are lo...

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“…For UV treatment (42), plates were washed with DPBS with calcium and magnesium (DPBSϩ). The DPBSϩ was removed, leaving a 1-mm-thick layer, and the cells were irradiated with 2,400 J of UV light/m 2 in a UV Stratalinker 2400 apparatus (Stratagene).…”

Section: Methodsmentioning

confidence: 99%

“…For enzymatic treatment of UV-irradiated DNA, 10 g of DNA was incubated in a 100-l reaction volume with T4 endonuclease V in 50 mM Tris-HCl (pH 7.6)-50 mM NaCl-1 mM EDTA-10 mM dithiothreitol (DTT)-100 g of bovine serum albumin/ml for 1 h at 37°C. Photolyase (Pharmingen) (5 g) was added under yellow light, and the DNA was incubated for 1 h at room temperature under black lights (42). The DNA was phenol extracted and ethanol precipitated.…”

Section: Methodsmentioning

confidence: 99%

Parent-of-Origin-Specific Binding of Nuclear Hormone Receptor Complexes in the H19-Igf2 Imprinting Control Region

Szabó

Pfeifer

Mann

2004

Molecular and Cellular Biology

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Parent-of-origin-specific expression of the mouse insulin-like growth factor 2 gene (Igf2) and the closely linked H19 gene located on distal chromosome 7 is regulated by a 2.4-kb imprinting control region (ICR) located upstream of the H19 gene. In somatic cells, the maternally and paternally derived ICRs are hypo-and hypermethylated, respectively, with the former binding the insulator protein CCCTC-binding factor (CTCF) and acting to block access of enhancers to the Igf2 promoter. Here we report on a detailed in vivo footprinting analysis-using ligation-mediated PCR combined with in vivo dimethyl sulfate, DNase I, or UV treatment-of ICR sequences located outside of the CTCF binding domains. In mouse primary embryo fibroblasts carrying only maternal or paternal copies of distal chromosome 7, we have identified five prominent footprints specific to the maternal ICR. Each of the five footprinted areas contains at least two nuclear hormone receptor hexad binding sites arranged with irregular spacing. When combined with fibroblast nuclear extracts, these sequences interact with complexes containing retinoic X receptor alpha and estrogen receptor beta. More significantly, the footprint sequences bind nuclear hormone receptor complexes in male, but not female, germ cell extracts purified from fetuses at a developmental stage corresponding to the time of establishment of differential ICR methylation. These data are consistent with the possibility that nuclear hormone receptor complexes participate in the establishment of differential ICR methylation imprinting in the germ line.

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UV Light as a Footprinting Agent: Modulation of UV-induced DNA Damage by Transcription Factors Bound at the Promoters of Three Human Genes

Cited by 125 publications

References 0 publications

Maximum likelihood analysis of mammalian p53 indicates the presence of positively selected sites and higher tumorigenic mutations in purifying sites

Maximum likelihood analysis of mammalian p53 indicates the presence of positively selected sites and higher tumorigenic mutations in purifying sites

A Novel Element and a TEF-2-like Element Activate the Major Histocompatibility Complex Class II Transactivator in B-lymphocytes

Parent-of-Origin-Specific Binding of Nuclear Hormone Receptor Complexes in the H19-Igf2 Imprinting Control Region

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