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PubMed1987

Lens-specific enhancer in the third intron regulates expression of the chicken delta 1-crystallin gene.

We have previously shown that the tissue specificity determinant of the chicken delta 1-crystallin gene lies 3' of position -100 (Hayashi et al. 1985). Since the promoter of the gene (delta 1-crystallin promoter) did not show any tissue specificity, we examined various segments of the delta 1-crystallin gene for a tissue-specific enhancer activity by placing each segment downstream of a heterologous transcriptional unit coding for chloramphenicol acetyltransferase (CAT) and by transfecting chicken tissues in primary culture. We found that a segment spanning the third intron bears a strong lens-specific enhancer activity. This "delta 1-crystallin enhancer" activates transcription from the delta 1-crystallin promoter 20- to 40-fold in lens cells and to various degrees with other promoters. Deletion analysis of the enhancer region indicated that it covered nearly 1 kb but did not indicate clear-cut boundaries. For its enhancer effect the core region of 120 bp and associations with certain adjoining regions were required. Removal of the enhancer from the gene totally abolished delta 1-crystallin expression, and reinsertion of the enhancer in either upstream, internal, or downstream positions restored expression. We conclude that the delta 1-crystallin enhancer is an essential and major determinant for lens-specificity of delta 1-crystallin expression.

Animals↗

PubMed1996

Transcriptional enhancers act in cis to suppress position-effect variegation.

We have examined the basis of enhancer effects on gene expression by altering the action of enhancers on expression of a stably integrated reporter gene. We used two distinct experimental approaches: recombinase-mediated deletion of an enhancer and modulation of the activity of another enhancer composed of downstream metal response elements (MREs). The flp recombinase was used to delete the 5'HS2 globin enhancer from a site downstream of beta-geo at nine separate integration sites in K562 erythroleukemia cells. In no case does deletion of 5'HS2 have a significant effect on the level of expression; however, the deletion does increase dramatically the rate at which expression of beta-geo is silenced. Zinc stimulation of a metallothionein enhancer has no effect on the level of reporter expression, but slows the rate of silencing. Silencing in both cases is highly site dependent, and resembles position-effect variegation (PEV). These results strongly support a binary mode of enhancer action, as in both cases the enhancer maintains reporter expression without a strong effect on the level of expression. Taken together, these findings suggest that transcriptional activators have a direct interaction with repressive chromatin structures, which is independent of an effect on the rate of transcription. We propose that cis-acting transcriptional control elements may act primarily through this mechanism.

Enhancer Elements, Genetic↗

PubMed1999

Nuclear matrix attachment regions antagonize methylation-dependent repression of long-range enhancer-promoter interactions.

The immunoglobulin intragenic mu enhancer region acts as a locus control region that mediates transcriptional activation over large distances in germ line transformation assays. In transgenic mice, but not in transfected tissue culture cells, the activation of a variable region (V(H)) promoter by the mu enhancer is dependent on flanking nuclear matrix attachment regions (MARs). Here, we examine the effects of DNA methylation, which occurs in early mouse development, on the function of the mu enhancer and the MARs. We find that methylation of rearranged mu genes in vitro, before transfection, represses the ability of the mu enhancer to activate the V(H) promoter over the distance of 1.2 kb. However, methylation does not affect enhancer-mediated promoter activation over a distance of 150 bp. In methylated DNA templates, the mu enhancer alone induces only local chromatin remodeling, whereas in combination with MARs, the mu enhancer generates an extended domain of histone acetylation. These observations provide evidence that DNA methylation impairs the distance independence of enhancer function and thereby imposes a requirement for additional regulatory elements, such as MARs, which facilitate long-range chromatin remodeling.

Acetylation↗

PubMed1988

The need for enhancers is acquired upon formation of a diploid nucleus during early mouse development.

The activity of the polyoma virus (PyV) origin of DNA replication was used as a sensitive assay for enhancer function in one- and two-cell mouse embryos by injecting embryos with plasmid DNA containing different PyV ori configurations, allowing them to continue development in vitro, and then measuring plasmid DNA replication. Replication always required the PyV origin 'core' sequence in cis and PyV large tumor antigen (T-Ag) in trans. In developing two-cell embryos, DNA replication also required an enhancer in cis. Two copies of part of PyV enhancer 3 (beta element) was sevenfold better than one copy, and enhancer 3 was better than enhancer 1 + 2 (alpha element). Competition between ori configurations suggested that enhancers bound specific proteins required for replication and transcription. In contrast, DNA injected into one-cell embryos did not need an enhancer for replication, and no competition for replication factors was observed between different ori configurations. In fact, ori core replicated about ninefold better in one-cell embryos than the complete origin did in developing two-cell embryos. Therefore, core contains all the cis-acting information necessary to initiate DNA replication. Because one-cell embryos that replicated injected DNA retained their pronuclei and remained one-cell embryos, enhancers are not needed in mammalian development until a diploid nucleus is formed.

Animals↗

PubMed1990

A novel enhancer in the immunoglobulin lambda locus is duplicated and functionally independent of NF kappa B.

As a first step toward defining the elements necessary for lambda immunoglobulin gene regulation, DNase I hypersensitive sites were mapped in the mouse lambda locus. A hypersensitive site found 15.5 kb downstream of C lambda 4 was present in all the B-cell but not in the T-cell lines tested. This site coincided with a strong B-cell-specific transcriptional enhancer (E lambda 2-4). This novel enhancer is active in myeloma cells, regardless of the status of endogenous lambda genes, but is inactive in a T-cell line and in fibroblasts. The enhancer E lambda 2-4 functions in the absence of the transcription factor NF kappa B, which is necessary for kappa enhancer function. No evidence could be found for NF kappa B binding by this element. Rearrangement of V lambda 2 to JC lambda 3 or JC lambda genes deletes E lambda 2-4; however, a second strong enhancer was found 35 kb downstream of C lambda 1, which cannot be eliminated by lambda gene rearrangements. The second lambda enhancer (E lambda 3-1) is 90% homologous to the E lambda 2-4 sequence in the region determined to comprise the active enhancer and likewise lacks the consensus binding site for NF kappa B. The data support a model for the independent activation of kappa and lambda gene expression based on locus-specific regulation at the enhancer level.

Animals↗

PubMed2006

Gray-level grouping (GLG): an automatic method for optimized image contrast enhancement--Part II: the variations.

This is Part II of the paper, "Gray-Level Grouping (GLG): an Automatic Method for Optimized Image Contrast Enhancement". Part I of this paper introduced a new automatic contrast enhancement technique: gray-level grouping (GLG). GLG is a general and powerful technique, which can be conveniently applied to a broad variety of low-contrast images and outperforms conventional contrast enhancement techniques. However, the basic GLG method still has limitations and cannot enhance certain classes of low-contrast images well, e.g., images with a noisy background. The basic GLG also cannot fulfill certain special application purposes, e.g., enhancing only part of an image which corresponds to a certain segment of the image histogram. In order to break through these limitations, this paper introduces an extension of the basic GLG algorithm, selective gray-level grouping (SGLG), which groups the histogram components in different segments of the grayscale using different criteria and, hence, is able to enhance different parts of the histogram to various extents. This paper also introduces two new preprocessing methods to eliminate background noise in noisy low-contrast images so that such images can be properly enhanced by the (S)GLG technique. The extension of (S)GLG to color images is also discussed in this paper. SGLG and its variations extend the capability of the basic GLG to a larger variety of low-contrast images, and can fulfill special application requirements. SGLG and its variations not only produce results superior to conventional contrast enhancement techniques, but are also fully automatic under most circumstances, and are applicable to a broad variety of images.

Algorithms↗

PubMed1990

A factor known to bind to endogenous Ig heavy chain enhancer only in lymphocytes is a ubiquitously active transcription factor.

The transcriptional enhancer located in the first intron of the immunoglobulin heavy chain constant region is a major determinant of B-cell-specific expression of immunoglobulin genes. Like other enhancers, the Ig heavy chain enhancer contains several short sequence motifs that bind specific transcription factors. Each binding site contributes to the overall activity of the enhancer, however no single element seems absolutely required for activity. For a better understanding of the Ig heavy chain enhancer components, we have cloned and analyzed individual sequence elements. We find that the factor that binds to the E3 enhancer motif, CATGTGGC, is a ubiquitous transcription factor. It is present in an active form in both B cells and non-B cells, where it can mediate transcriptional activation in vitro and in vivo. However, despite its ability to activate transcription of a transfected reporter gene, the factor is apparently unable to bind to the endogenous Ig heavy chain enhancer in non-lymphoid cells: In previous experiments by others, the characteristic in vivo footprint of this factor, designated NF-muE3, was detected in B cells but not in non-B cells. From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B lymphocytes: (a) cell-specific factors such as Oct-2A and Oct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as NF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors, exemplified by the one binding to the E3 sequence motif. This factor is present in an active form in a variety of cell types but is apparently unable to bind to the endogenous Ig heavy chain enhancer in non-B cells, perhaps due to a non-permissive chromatin structure of the Ig heavy chain locus.

B-Lymphocytes↗

PubMed2001

A model of the real-time correlation of viral titers with immune reactions in antibody-dependent enhancement of dengue-2 infections.

We simultaneously assessed dengue-2 virus (DEN-2) titers by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and immune reactions including interleukin-4 (IL-4), interferon-gamma (IFN-gamma) and prostaglandin E(2) (PGE(2)) production by human mononuclear cells (MNLs) in a model of antibody-dependent enhancement (ADE). We found that DEN-1 immune sera at 1:100 and 1:250, but not those at 1:10 or control sera, enhanced DEN-2 infections in human MNLs as assessed by the fluorogenic RT-PCR technique. The enhanced profiles of DEN-2 infections determined by the RT-PCR in 6 h were reproducible by the standard plaque-forming unit (PFU) measurement established after 7 days. The ADE-enhanced DEN-2 titers determined by the RT-PCR were 5.5-33-fold higher than those detected by PFU assay, suggesting that total virions during infections were much higher than the viable ones detected by PFU assay. MNLs in response to DEN-2 infections had higher IFN-gamma and PGE(2) production. However, the enhancement of DEN-2 infections by DEN-1 immune sera in MNLs was not associated with further enhancement of IFN-gamma production. In contrast, the presence of subneutralizing DEN-1 immune sera that enhanced DEN-2 infections also enhanced PGE(2) but not IL-4 production. The results of this study suggest that ADE of DEN-2 infections associated with induction of immunosuppressive mediators such as PGE(2) and IL-4 can be simultaneously assessed in a real-time fashion.

Antibody-Dependent Enhancement↗

PubMed1985

Long-term passive enhancement of allogeneic skin grafts with monoclonal antibodies.

Monoclonal antibodies (mAb) to graft-specific class I or class II major histocompatibility antigens were tested for their ability to enhance the survival of allogeneic skin transplants. Mutant mouse strains were grafted with wild type tissue to restrict the antigenic differences being recognized. For allogeneic recognition of the class I antigen Ld, mutant BALB/c-H-2dm2 (dm2) mice were grafted with wild type BALB/cKh skin, and two dm2 anti-BALB/cKh mAb, 23-10-1 and 30-5-7, were tested for their ability to enhance. The anti-Ld antibody 23-10-1 (IgM) was found not to enhance the survival of BALB/c skin on dm2 mice. 30-5-7, however, an IgG2a antibody of indistinguishable specificity from 23-10-1, prolonged graft survival for approximately 5 days. For recognition of selected Iab determinants, mutant B6.C-H-2bm12 (bm12) mice were grafted with wild type B6/Kh skin, and mAb specific for the serological change(s) in bm12 were tested for their ability to enhance. The anti-Iab antibody 25-9-17 (IgG2a) was found not to enhance B6 grafts on bm12 mice. However, the enhancement seen with 25-9-17 using (C3H X bm12)F1 recipients was extraordinary, such that treated mice had a mean survival time three times that of the controls. Since 25-9-17 is of C3H origin, these results suggest that allotype (or possibly idiotype) compatibility is important in antibody enhancement. Another anti-Iab antibody 28-16-8 (IgM), also of C3H origin, failed to enhance a B6 graft on (C3H X bm 12)F1 mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

An RNA polymerase-binding protein that is required for communication between an enhancer and a promoter.

Although bacteriophage T4 late promoters are selectively recognized by Escherichia coli RNA polymerase bearing a single protein encoded by T4 gene 55 (gp55), efficient transcription at these promoters requires enhancement by the three T4 DNA polymerase accessory proteins, bound to distal "mobile enhancer" sites. Two principles are shown to govern this transcriptional enhancement: (i) Promoter recognition and communication between the enhancer and the promoter require separate phage-coded proteins. Only RNA polymerase that has the T4 gene 33 protein (gp33) bound to it is subject to enhancement by the three DNA replication proteins. (ii) Transcriptional enhancement in this prokaryotic system is promoter-specific. Promoter specificity is generated by a direct competition of phage T4 gp33 and gp55 with the E. coli promoter recognition protein, sigma 70, for binding to the E. coli RNA polymerase core. Thus, polymerase that contains sigma 70 is competent to transcribe T4 early and middle genes, but lacks the ability to be enhanced by the DNA replication proteins, while polymerase that contains gp55 and gp33 is capable of enhancement via gp33, but its activity is restricted to T4 late promoters by gp55.

Carrier Proteins↗

PubMed1987

Protein-binding sites in Ig gene enhancers determine transcriptional activity and inducibility.

Individual protein-binding sites within the mouse immunoglobulin heavy chain and kappa light chain gene enhancers were altered, making it possible to examine the functional role of the sites during transcription. The E motifs, which bind factors that are present in many if not all cells, mostly behave as transcriptional activating sites. The only known heavy chain enhancer site that binds a lymphocyte-specific factor, the "octamer" site, plays a critical role in transcription but only in a truncated form of the enhancer. In the full enhancer, no one site is crucial because of an apparent functional redundancy. The site in the kappa enhancer that binds a factor specific to mature B cells, kappa B, was crucial to the constitutive activity of the enhancer in B cells. This factor is also inducible in pre-B cells, and the site was necessary for inducibility of the kappa enhancer. Thus, the sites defined by protein binding are important for the functional activity of immunoglobulin enhancers, with the sites that bind proteins restricted in their cellular distribution playing the most important roles.

Animals↗

PubMed1988

Properties of the human hepatitis B virus enhancer: position effects and cell-type nonspecificity.

The genome of human hepatitis B virus (HBV) contains an enhancer element within a 360-base-pair transcribed region located between sequences encoding the virus surface and core antigens. Beyond the usual properties associated with enhancers (i.e., activity 5' or 3' of a heterologous promoter and relative orientation independence), DNA sequences encompassing this enhancer exhibited unexpected characteristics. Using gene expression assays in both stably and transiently transfected cells, we found that the HBV enhancer element, when located in a transcribed region of chimeric genes, dramatically increased expression levels of genes controlled by the simian virus 40 promoter/enhancer. This synergism was not observed, however, when the HBV enhancer was located outside of the transcribed region. When these transcribed sequences were reversed in orientation, expression levels decreased significantly. These data suggest that RNA stability and transcriptional activity may be affected by sequences associated with this DNA region. In contrast to the findings of others, we found that the HBV enhancer activated transcription in a relatively cell-type-independent manner when the enhancer was located either 5' of the promoter or in the 3' untranslated region of gene constructs. The implications of these and other properties of the HBV enhancer region on viral gene expression and its life cycle are discussed.

Animals↗

PubMed1989

Characterization of enhancer elements and their mutations in the long terminal repeat of feline endogenous RD-114 proviruses.

To locate the enhancer regions of the feline endogenous RD-114 long terminal repeat (LTR), we examined expression of the chloramphenicol acetyltransferase gene driven by various segments of the U3 region from two different proviral loci (CRL3 and CR1). Transient expression assays demonstrated that the primary signal sequence for transcription enhancement was located within the 63-base-pair (bp) element of the CRL3 DNA occurring between positions -184 and -121 from the CAP site (+1), whereas the similar region of CR1 was almost inactive. This element from both CRL3 and CR1 contained a single 30-bp sequence (direct repeat [DR]-B2) found in duplicate tandem copies in the LTR of the infectious RD-114 provirus. Two 9-bp inverted repeats marked the DR-B unit of the active element, and a prominent base deletion in one of these repeats in CR1 DNA appeared to be related to loss of enhancer activity. Another segment of CRL3 (-296 to -184), also displaying enhancer function, contained tandem repeated sequences (DR-A1 and DR-A2). The Dr-A2 unit, which lacked the 5' 20-bp sequence of the 47-pb DR-A1, could not function as an enhancer by itself, but it contributed to enhancer effects in cooperation with either the DR-A1 or DR-B2 region. The CR1 LTR contained a single DR-A1 sequence with extensive mutations, and the region (-313 to -181) containing this DR-A1 unit was nonfunctional, similar to the DR-B2 region of CR1. Site-directed mutagenesis analysis of another enhancer element, an octamer motif occurring between CAAT and TATA boxes of all RD-114 LTRs sequenced, revealed that this element was necessary for full enhancer function of the U3 region but with a variable effect, depending on the cell types in which chloramphenicol acetyltransferase expression was determined.

Animals↗

PubMed1990

Genetic analysis of the enhancer requirements for polyomavirus DNA replication in mice.

In this report, we describe the first systematic analysis of the genetic requirements for polyomavirus (Py) enhancer-activated viral DNA replication during the acute phase of infection in mice. Four mutants were made which substituted XhoI sites for conserved enhancer consensus sequences (adenovirus type 5 E1A, c-fos, simian virus 40, and a glucocorticoidlike consensus sequence). Viral DNA replication in infected mouse organs was measured by DNA blot analysis. Only the loss of the glucocorticoidlike consensus sequence element significantly reduced Py DNA replication in the kidneys, the primary target organ for viral replication. The loss of the c-fos, adenovirus type 5 E1A, or simian virus 40 consensus sequences, however, expanded organ-specific viral DNA replication, relative to wild-type Py, by allowing high-level replication in the pancreas or heart or both. Analysis of Py variants selected for replication in undifferentiated embryonal carcinoma cell lines (PyF441, PyF111) showed that there was little change in levels of viral DNA replication in kidneys and other organs as compared with those in the wild-type virus. If the entire B enhancer is deleted, only low overall levels of viral replication are observed. Wild-type levels of replication in the kidneys can be reconstituted by addition of a single domain from within the A enhancer (nucleotides 5094 to 5132) to the B enhancer deletion virus, suggesting that a single domain from the A enhancer can functionally substitute for the entire B enhancer. This also indicates that the determinants for kidney-specific replication are not found in the B enhancer.

Animals↗

PubMed1992

Down-regulation of the major histocompatibility complex class I enhancer in adenovirus type 12-transformed cells is accompanied by an increase in factor binding.

In transformed cells, the E1A gene of adenovirus type 12 (Ad12) represses transcription of class I genes of the major histocompatibility complex. The tumorigenic potential of Ad12-transformed cells correlates with this diminished class I expression. In contrast, the E1A gene of the nontumorigenic Ad5 does not affect class I expression. We show here that a transfected reporter chloramphenicol acetyltransferase plasmid driven by an H-2K promoter (-1049 bp) was expressed at much lower levels in Ad12- than in Ad5-transformed mouse cells. Analysis of mutant constructs revealed that only 83 bp of H-2 DNA, consisting of the enhancer juxtaposed to the basal promoter, was sufficient for this differential expression. Whereas the H-2 basal promoter alone was somewhat less active in Ad12-transformed cells, the H-2 TATA box itself did not appear to be important. The H-2 enhancer proved to be the principal element in Ad12 E1A-mediated repression, since (i) substitution of the H-2 enhancer by simian virus 40 enhancers overcame the repression, and (ii) when juxtaposed to either its native or heterologous basal promoters, the H-2 enhancer was functional in Ad5- but not Ad12-transformed cells. Mobility shift assays showed that there is a DNA-binding activity to the 5' site (R2 element) of the enhancer that is significantly higher in Ad12- than in Ad5-transformed cells. These results suggest that decreased class I enhancer activity in Ad12-transformed cells may, at least in part, be due to the higher levels of an enhancer-specific factor, possibly acting as a repressor.

Adenovirus E1A Proteins↗

PubMed1992

The bovine papillomavirus constitutive enhancer is essential for viral transformation, DNA replication, and the maintenance of latency.

Bovine papillomavirus type 1 (BPV-1) has served as the prototype papillomavirus for the study of viral transcription, DNA replication, and latency. However, no cis essential transcription control regions which are necessary for both transformation and replication of BPV-1 or any other papillomavirus have yet been defined. We have found that BPV-1 mutants with deletions in the long control region were defective for transformation and replication, with the essential region in the 5' long control region corresponding to the previously defined BPV-1 constitutive enhancer (S. B. Vande Pol and P. M. Howley, J. Virol. 64:5420-5429, 1990). BPV-1 mutants deleted of the constitutive enhancer could be complemented in trans by the full-length virally encoded E2 transactivator and replication factor (E2TA) and in cis by the simian virus 40 enhancer. The constitutive enhancer induced the production of E2TA by activating all the major viral early promoters upstream of the E2 open reading frame. Complementation experiments using a temperature-sensitive E2TA mutant indicated that the constitutive enhancer was necessary for the maintenance of viral DNA replication within latently infected cells and implied that viral transcription under the regulation of the constitutive enhancer may be controlled during the cell cycle. The constitutive enhancer is a master regulatory control region for establishing and maintaining BPV-1 latency, and its characteristics reveal some analogies with cell type-specific enhancer elements recognized in the human papillomaviruses.

Animals↗

PubMed1992

Activation of the human immunodeficiency virus type 2 enhancer is dependent on purine box and kappa B regulatory elements.

Human immunodeficiency virus type 2 (HIV-2) displays several features which distinguish it from HIV-1. Among the differences in these two viruses are the responses of their enhancer regions to T-cell activation. For example, stimulation of HIV-1 transcription is largely dependent on two kappa B regulatory elements. In contrast, the HIV-2 enhancer has a single kappa B site and contains additional cis-acting sequences responsive to induction. One of these sites, previously termed CD3R, is a purine-rich site, also called PuB1, which is responsive to stimulation of the CD3 component of the T-cell receptor complex and binds Elf-1, a member of the ets proto-oncogene family. In this report, we examine the interaction of the PuB1 site with other sites in the HIV-2 enhancer. We demonstrate that the PuB1 site confers responsiveness to T-cell activators only in cooperation with additional enhancer elements. Induction of the HIV-2 enhancer is dependent on at least two other cis-acting regulatory elements in addition to PuB1 and kappa B. One of these elements is another purine-rich site (PuB2), which also binds recombinant Elf-1. An adjacent region, proximal to the PuB2 ets (pets) site, shows protection in DNase footprinting experiments with extracts from Jurkat T cells. Mutation of either the kappa B, PuB1, PuB2, or pets site significantly reduces the response of the HIV-2 enhancer to T-cell stimulation, an effect which is mediated at the RNA level. Therefore, activation of the HIV-2 enhancer is dependent on at least four cis-acting elements, only one of which is found in HIV-1, which act in synergy with one another. Despite their sequence similarity, the organization and function of the HIV-2 enhancer have diverged considerably from those of HIV-1.

Base Sequence↗

PubMed1993

Binding of nuclear factors to functional domains of the duck hepatitis B virus enhancer.

We have analyzed the structures, relative organization, and activities of binding sites for nuclear factors in the duck hepatitis B virus (duck HBV) enhancer. DNase I footprinting analysis and mobility shift assays demonstrate that this enhancer of 192 bp contains at least three binding sites for transcription factors: one for hepatocyte-adipocyte C/EBP, a second for the liver-specific transactivator hepatocyte nuclear factor 1 HNF-1, and a third for a factor, called F3, which binds to a DNA sequence bearing some resemblance to that for the ubiquitous factor EF-C. Analysis of transcriptional activity reveals that oligonucleotides corresponding to the individual binding sites, inserted upstream from a heterologous promoter, display very weak enhancer activity, whereas the enhancer encompassing these three sites displays very high activity. Analysis of duck HBV enhancer mutants indicates that the deletion of any of these sites leads to a modification of transcriptional enhancer activity. The hepatocyte nuclear factor 1 binding site is crucial, since an internal deletion of 14 bp abolishes the activity. The C/EBP site can act as repressor, and the F3 site is required for full activity. Comparative analysis reveals that the nuclear factors are similar to those bound to the human HBV enhancer but that the organization of their binding sites in the duck HBV enhancer is different.

Animals↗