Inherited immunodeficiency with a defect in a major histocompatibility complex class II promoter-binding protein differs in the chromatin structure of the HLA-DRA gene.

Gönczy, Pierre; Reith, Walter; Barras, Emmanuèle; Lisowska-Grospierre, B; Griscelli, C; Hadam, M.; Mach, Bernard

doi:10.1128/mcb.9.1.296

Cited by 40 publications

(28 citation statements)

References 47 publications

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“…The same polymorphism is observed with DNA from FS2 cells, while HeLa cell DNA has only the site at -2400 (Pine, unpublished data (9). In cells that express the factor RF-X, a constitutive hypersensitive site exists where RF-X binds to the X box in the promoter region of the HLA-DRA gene (13). Proteins bound in vitro to chicken 3-globin promoter sequences create close-by hypersensitive sites (7,8).…”

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confidence: 62%

“…Proteins that bind in vitro to the ISRE of ISG15 and ISG54 (20,21,26) and to other ISRE sequences (3,16,18,32,37) (5,6,14,30,33,41,42). Constitutive DNase-hypersensitive sites are often found in genes that are poised for inducible transcription (2,10,13,27,39,43,45), and such constitutive sites can be enhanced or new sites can appear when such genes are actively transcribed. The Drosophila heat shock genes provide a well-documented case in which proteins bound at regulatory sites influence DNase hypersensitivity (36,40,44).…”

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confidence: 99%

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In vivo evidence of interaction between interferon-stimulated gene factors and the interferon-stimulated response element.

Pine¹,

Darnell²

1989

Mol. Cell. Biol.

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Constitutive and interferon-inducible DNase hypersensitive sites in vivo are located in interferon-stimulated gene promoters near sequences that specifically bind constitutive or interferon-inducible proteins in vitro. Induced sites and proteins are transient or maintained, depending on cell type. Interferon-stimulated gene transcription is transient or maintained in parallel.Interferon-stimulated-genes (ISGs) are transcriptionally activated when alpha interferon (IFN-ox) binds to their cell surface receptors (1,12,(23)(24)(25)34). An IFN-stimulated response element (ISRE) was precisely defined by deletions and point mutations in the promoters of ISG15 and ISG54 (20,25,26,34), and a similar sequence has been identified in other ISGs (3,16,17,22,32,37,38). Proteins that bind in vitro to the ISRE of ISG15 and ISG54 (20,21,26) and to other ISRE sequences (3,16,18,32,37) (5,6,14,30,33,41,42). Constitutive DNase-hypersensitive sites are often found in genes that are poised for inducible transcription (2,10,13,27,39,43,45), and such constitutive sites can be enhanced or new sites can appear when such genes are actively transcribed. The Drosophila heat shock genes provide a well-documented case in which proteins bound at regulatory sites influence DNase hypersensitivity (36,40,44). Inducible sites have also been identified in the promoters of the interleukin-2 gene (39) and the IFN--y-inducible gene IPIO (27), among others. Examination of the relation among ISG chromatin structure, specific transcription factors, and transcription suggests that ISGFs act in vivo through ISRE. ). In all these cases, transcription peaks between 0.5 and 2 h after addition of IFN-(x to cells. A decline to nearly basal levels after 6 to 12 h in the continuous presence of IFN-a partly depends on new protein synthesis. The level of the response is not maximal unless the cells are treated with at least 250 to 500 U of IFN-a per ml. As for all other responsive cells tested, induction of Daudi cell ISG transcription also occurs within 15 min after treatment with IFN-a. However, Daudi cells are distinguished by their response to as little as 5 U of IFN-a per ml, and run-on transcription assays (24) done with ISG and control probes previously described (31) showed that induction of the ISGs did not decline at later times but remained high after 6, 12, or 20 h in the continuous presence of IFN-a (data not shown). This result was consistent with the persistence of induced ISG mRNA in Daudi cells (21,29).The presence of promoter-binding factors parallels transcription in each cell type. We wished to compare the presence of ISGF in WI38VA and Daudi cells particularly, because of the prolonged IFN-ox-induced ISG transcription in Daudi cells. Each cell type was treated for various lengths of time with IFN-a, and nuclear extracts were prepared essentially as described elsewhere (4). Some Daudi cell samples were also treated with cycloheximide before extracts were prepared. Specific DNA-binding proteins were then detected as previously described (26) wi...

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confidence: 62%

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confidence: 99%

In vivo evidence of interaction between interferon-stimulated gene factors and the interferon-stimulated response element.

Pine¹,

Darnell²

1989

Mol. Cell. Biol.

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“…In both of these cases the open architecture of the relevant promoters is established by a second transcription factor, whose expression precedes the expression of the transactivator. Thus, regulatory factor X is responsible for establishing the DHS at the HLA-DRA promoter (69) whereas GAGA factor performs the same role at heat shock gene promoters (70,71). A logical extension of these observations is that there may be a transcription factor that binds to p53-regulated promoters and establishes the open chromatin confirmation prior to p53 activation.…”

Section: Fig 6 P53 Interacts With P53 Res In Dna-damaged Hct116 Celmentioning

confidence: 84%

Constitutive DNase I Hypersensitivity of p53-Regulated Promoters

Braastad

Han

Hendrickson

2003

Journal of Biological Chemistry

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The ability of p53 to alter, at the transcriptional level, the gene expression of downstream targets is critical for its role as a tumor suppressor. Most models of p53 activation postulate the stepwise recruitment by p53 of coactivators, histone acetyltransferases, and/or chromatin remodeling factors to a promoter region to facilitate the subsequent access of the general transcriptional machinery required for transcriptional induction. We demonstrate here, however, that the promoter regions for the p53 target genes, p21, 14-3-3, and KARP-1, exist in a constitutively open conformation that is readily accessible to DNase I. This conformation was not altered by DNA damage or by whether p53 was present or absent in the cell. In contrast, p53 response elements, which resided outside the immediate promoter regions, existed within DNase I-resistant chromatin domains. Thus, p53 activation of downstream target genes occurs without p53 inducing chromatin alterations detectable by DNase I accessibility at either the promoter or the response element. As such, these data support models of p53 activation that do not require extensive chromatin alterations to support cognate gene expression.The differential chromatin structure and nuclease accessibility at a promoter region has long been recognized as a key distinguishing feature between active and inactive genes (reviewed in Ref. 1). Almost invariably, the promoter regions of active genes are marked experimentally by hypersensitivity to restriction endonucleases (2, 3) or, more commonly, DNase I (4). Although this hypersensitivity can be caused by torsional or topological stress in the DNA and distortions in the chromatin structure resulting from transcription factor binding, it is generally caused by the absence of nucleosomes or their remodeling (1, 4). The paucity of nucleosomes, in turn, is a direct consequence of the repressive effect that nucleosomes have on the transcriptional machinery and the requirement to alleviate that effect for productive transcription to occur (5-7). Thus, inactive genes usually have promoters that are nucleosomal, are insensitive to DNase I, and are regarded as being in a closed confirmation whereas active genes usually have core promoters that are nucleosome-free, hypersensitive to DNase I, and in an open configuration. Consequently, one of the hallmarks of gene induction mechanisms is the remodeling of the nucleosomal architecture of a promoter as it is activated (5, 6, 8).Enormous strides have been made in the last decade in understanding transcriptional activation at the chromatin level. In particular, the activation of expression of many, although not all (9 -11), inducible eukaryotic genes is consistent with what can collectively be called recruitment models of gene activation (3, 7, 8) (reviewed in Ref. 12). These models usually require, in response to some extracellular cue, the induction of a specific transcription factor and the subsequent interaction of that factor with its cognate response element, which is invariably a cis-acting ...

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“…There is also significantly reduced or absent promoter occupancy in cells from patients with bare lymphocyte syndrome (BLS), where RFX is defective or missing (26)(27)(28). In BLS cells, the HLA-DRA promoter DNase I-hypersensitive site is absent (17), indicating a close association of nucleosomes with promoter DNA.…”

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Histone Deacetylase Activity Represses Gamma Interferon-Inducible HLA-DR Gene Expression following the Establishment of a DNase I-Hypersensitive Chromatin Conformation

Osborne¹,

Zhang²,

Yang

et al. 2001

Molecular and Cellular Biology

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Expression of the retinoblastoma tumor suppressor protein (Rb) is required for gamma interferon (IFN-␥Major histocompatibility complex (MHC) class II molecules are heterodimeric cell surface glycoproteins comprised of both a heavy (alpha) chain and a light (beta) chain. MHC class II molecules (HLA-DR, -DP, and -DQ in humans) bind and display peptide antigens for recognition by CD4 ϩ T lymphocytes. Recognition of the MHC class II heterodimer-antigen complex by the T-cell receptor and the accessory protein CD4 of T lymphocytes leads to the generation of an immune response. MHC class II molecules play an important role in antitumor immunity (1-4, 11, 29, 42-44, 49). Specifically, transfection of tumor cells with syngeneic murine MHC class II genes immunizes mice against MHC class II-negative parental tumor cells (2). Vaccination of mice using this protocol also leads to eradication of an MHC class II-negative, basement membrane-invasive tumor (4). Also, tumor-specific antigens capable of eliciting HLA class II-restricted activation of tumorinfiltrating T lymphocytes have been identified (46,57,58).MHC class II expression is constitutively activated during development in professional antigen-presenting cells, such as B cells, dendritic cells, and macrophages; it is inducible by cytokines, most importantly, gamma interferon (IFN-␥), in nearly all other types of cells. MHC class II expression is regulated primarily at the level of transcription through promoter elements that are conserved among the MHC class II genes and the genes encoding accessory molecules such as the invariant chain, the MHC class II chaperone. The elements are, from 5Ј to 3Ј, S box, X1 box, X2 box, Y box, and TATA box. The transactivators RFX, X2BP (CREB), and NF-Y are required factors for MHC class II gene activation and bind the X1, X2, and Y boxes, respectively. Cooperative interactions between transactivators bound to the X and Y elements have been demonstrated to be essential for the establishment of promoter occupancy and the transcription of class II genes (60). In particular, binding of the Y box factor, NF-Y, has been demonstrated to be required for occupancy of the other promoter elements and for IFN-␥-inducible MHC class II gene expression (60). In addition to the promoter binding factors, the class II transactivator (CIITA) is a required coactivator that functions by interaction with and stabilization of the transcription factors previously assembled on MHC class II promoters (20,24,38,53,59,68).It has been shown that the retinoblastoma tumor suppressor protein (Rb) is also required for IFN-␥-inducible MHC class II gene expression (34,35,41,67). Several Rb-defective human tumor cell lines exhibit a loss of IFN-␥-inducible MHC class II gene expression that is rescued by the reexpression of func-* Corresponding author. Mailing address:

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Inherited immunodeficiency with a defect in a major histocompatibility complex class II promoter-binding protein differs in the chromatin structure of the HLA-DRA gene.

Cited by 40 publications

References 47 publications

In vivo evidence of interaction between interferon-stimulated gene factors and the interferon-stimulated response element.

In vivo evidence of interaction between interferon-stimulated gene factors and the interferon-stimulated response element.

Constitutive DNase I Hypersensitivity of p53-Regulated Promoters

Histone Deacetylase Activity Represses Gamma Interferon-Inducible HLA-DR Gene Expression following the Establishment of a DNase I-Hypersensitive Chromatin Conformation

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