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PubMed1993

Formation of a cleavasome: enhancer DNA-2 stabilizes an active conformation of NaeI dimer.

Cleavage of DNA by NaeI-type restriction enzymes is stimulated by a DNA element with affinity for the activator site of the enzyme: a cleavage-enhancer DNA element. Measurements of the mobility of NaeI activity in comparison with protein standards on gel permeation columns and glycerol gradients demonstrated that NaeI, without enhancer, can form a 70,000 MW dimer. The dimer, however, is inactive: it could not cleave the "resistant" NaeI site in M13mp18 DNA in the absence of enhancer. In cleavage assays, enhancer stimulated either DNA nicking or DNA cleavage, depending upon NaeI concentration, and reduced the NaeI concentration required for the transition from nicking to cleavage activity. A gel mobility-shift assay of the interaction of NaeI with enhancer showed the formation of two complexes. Results using different sized DNAs and different percentage acrylamide gels for gel mobility-shift analysis implied that the two complexes were caused by NaeI monomer and dimer structures rather than one and two DNA binding. Dimer formation increased with the affinity of enhancer for NaeI. UV cross-linking "captured" the NaeI-enhancer complex; electrophoretic analysis of the cross-linked products showed NaeI dimer bound to enhancer. These results imply a model for cleavage enhancement in which enhancer binding stabilizes an active NaeI dimer conformation ("cleavasome") that cleaves both DNA strands before dissociating.

Base Sequence↗

PubMedDate not supplied

Invasive lobular carcinoma: spectrum of enhancement and morphology on magnetic resonance imaging.

Invasive lobular carcinoma (ILC) may be a difficult tumor to detect early by physical examination, mammography, or ultrasound. We undertook this study to describe the spectrum of gadolinium enhancement and morphologic features of ILC on magnetic resonance imaging (MRI). Nineteen patients with ILC who presented with a palpable mass, a mammographically visible abnormality, or an unknown primary underwent preoperative MRI of both breasts using a T1-weighted high-resolution gradient echo sequence (pre- and postcontrast), and an echoplanar sequence during the administration of gadolinium. Using a quantitative measure of gadolinium uptake over time, called the extraction flow (EF) product, and a normal tissue threshold EF level of 25 or less, enhancement for 15 of the 19 cancers was characterized. By consensus, three radiologists categorized the morphologic features of the lesions. For the 15 cases of ILC that had echoplanar data, analysis showed peak EFs ranging between 25 and 120, and the majority showed EFs in the 30s. A substantial portion of two tumors enhanced in a similar fashion to normal breast tissue, with EFs in the low 20s. Morphologically MRI showed a focal mass in eight cases, regional enhancement in five, segmental enhancement in one, segmental enhancement with multiple small nodules in one, a mixture of a focal mass and regional enhancement in one, diffuse enhancement in one, multiple small nodules in one, and bilateral disease in one. Of the focal masses, seven were irregular in shape and one was round; six had ill-defined margins and two had spiculated margins. All eight enhanced heterogeneously. Four cases had multifocal disease and one case had unsuspected contralateral disease discovered only on MRI. MRI using a combination of morphology and a quantitative measure of gadolinium uptake was able to detect the majority of cases of ILC. However, there was a variable morphologic appearance and contrast enhancement pattern on MRI. A few lesions were difficult to distinguish from normal tissue. This suggests that some cases of ILC may be difficult to detect on MRI.

Adult↗

PubMed1985

A long and complex enhancer activates transcription of the gene coding for the highly abundant immediate early mRNA in murine cytomegalovirus.

Using the simian virus 40 "enhancer trap" approach, we have identified a transcription enhancer located just upstream of the major immediate early gene of murine cytomegalovirus. This enhancer has several striking properties. (i) Together with the enhancer of human cytomegalovirus, it is the strongest transcription enhancer found to date. (ii) It is an extremely long enhancer, spanning greater than 700 base pairs. (iii) It consists of a rather complex pattern of sequence repeats, the longest of which is 181 base pairs. Also, several types of short sequence motifs are scattered throughout the enhancer in monomeric, heterodimeric, or homodimeric (palindromic) form. These motifs have been identified to be components of other enhancers and promoters, and they are presumably binding sites for specific nuclear factors. Our analysis suggests that enhancers are composed of a modular arrangement of short conserved sequence motifs and that enhancer strength is correlated with the redundancy of these motifs.

Animals↗

PubMed1986

Activation of gene expression is adversely affected at high multiplicities of linked simian virus 40 enhancer.

We have cloned multiple copies of 72-base-pair (bp) repeat transcriptional enhancer element from simian virus 40 in plasmid vectors upstream from the bacterial chloramphenicol acetyltransferase gene under the control of the simian virus 40 early promoter. Two copies of the 72-bp repeat provided efficient activation of gene expression. Increasing the number of linked 72-bp units to four substantially improved the activation of gene expression, but further addition of enhancers diminished the activation of gene expression proportionally to the number of enhancers added. Enhancer regions containing 10 or more copies of the 72-bp sequence were very inefficient in gene activation. Plasmids containing such expanded enhancer regions also competed less efficiently in vivo for trans-acting enhancer-binding factors. These effects are specific for the enhancer element and are not produced by reiterations of the 21-bp promoter element. Multiple enhancer units placed upstream do not interfere with the accuracy of mRNA initiation directed by the simian virus 40 early promoter in these plasmid constructs but do severely inhibit the initiation of replication at the neighboring simian virus 40 origin of replication that overlaps the early promoter region. These results are consistent with the hypothesis that the structural alterations induced in the DNA by a large number of copies of the enhancer are not favorable for the activation of a linked gene or for the binding of factors believed to mediate the enhancement effect.

Acetyltransferases↗

PubMed1988

A beta-cell-specific protein binds to the two major regulatory sequences of the insulin gene enhancer.

The selective transcription of the Rat insulin 1 gene is mainly dependent on a beta-cell-specific enhancer element located in the 5' flanking DNA. In analogy to many other viral and cellular enhancers, the insulin enhancer has been shown to be of a mosaic structure and the cis-acting elements of importance for the enhancer activity have been defined. Two short sequences are of crucial importance for the enhancer activity since mutation of either sequence leads to a decrease in activity (by a factor of approximately 10), and the double mutant eliminates all enhancer activity. This study shows that these two major cis-acting elements interact with beta-cell-specific proteins. These two enhancer modules carry an 8-base-pair homology and compete with each other for protein binding, suggesting that they interact with the same protein, designated insulin enhancer binding factor 1 (IEF 1). Since mutation of these sequences eliminates the enhancer activity and protein binding, we propose that IEF 1 is the key regulator controlling the selective activity of the insulin gene enhancer.

Animals↗

PubMed1988

Mutational analysis of the chicken beta-globin enhancer reveals two positive-acting domains.

We report a mutational analysis of the chicken beta-globin enhancer, using transient expression in primary embryonic erythrocytes. A series of 27 scanning mutants differing only by consecutive 4-base substitutions was tested. Previous experiments, using protection from DNase I digestion, demonstrated four regions in the enhancer that bind factors. Mutations in two of the four regions (denoted I and III) have no effect on enhancer activity. The other two regions (II and IV) mediate all of the positive-acting activity. Region II appears to consist of two subregions, mutation in either of which leads to the same loss in activity as mutation of both. Like region II, mutation of either half of region IV results in reduced enhancer activity. However, in contrast to region II, mutation of both halves of region IV results in more loss of enhancer activity than either single mutation. These data suggest that the half-sites in region II must interact in order to cause enhancement, whereas the half-sites in region IV act independently. Triplications of regions II or IV are able to enhance to a similar degree as the parental enhancer, but single copies of regions II or IV enhance only weakly. Thus, as measured by transient expression in embryonic erythrocytes, the beta-globin enhancer may involve the action of as few as three DNA-binding proteins acting at two sites.

Acetyltransferases↗

PubMed1997

Transactivation of an intronic hematopoietic-specific enhancer of the human Wilms' tumor 1 gene by GATA-1 and c-Myb.

The Wilms' tumor 1 gene (WT1) encodes a zinc-finger transcription factor which is expressed in a tissue-specific manner. Our studies indicate that in addition to the promoter, other regulatory elements are required for tissue-specific expression of this gene. A 258-base pair hematopoietic specific enhancer in intron 3 of the WT1 gene increased the transcriptional activity of the WT1 promoter by 8-10-fold in K562 and HL60 cells. Sequence analysis revealed both a GATA and a c-Myb motif in the enhancer fragment. Mutation of the GATA motif decreased the enhancer activity by 60% in K562 cells. Electrophoretic mobility shift assays showed that the GATA-1 protein in K562 nuclear extracts binds to this motif. Cotransfection of the enhancer containing reporter construct with a GATA-1 expression vector showed that GATA-1 transactivated this enhancer, increasing the CAT reporter activity 10-15-fold. Similar analysis of the c-Myb motif by cotransfection with the enhancer CAT reporter construct and a c-Myb expression vector showed that c-Myb transactivated the enhancer by 5-fold. A DNase I-hypersensitive site has also been mapped in the 258-base pair enhancer region. These data suggest that GATA-1 and c-Myb are responsible for the activity of this enhancer in hematopoietic cells and may bind to the enhancer in vivo.

Base Sequence↗

PubMed1999

Lack of enhancer function in mammals is unique to oocytes and fertilized eggs.

Previous studies have shown that the lack of novel coactivator activity in mouse oocytes and one-cell embryos (fertilized eggs) renders them incapable of utilizing Gal4:VP16-dependent enhancers (distal elements) but not promoters (proximal elements) in regulating transcription. This coactivator activity first appears in two- to four-cell embryos coincident with the major activation of zygotic gene expression. Here we show that whereas oocytes and fertilized eggs could utilize Sp1-dependent promoters, they could not utilize Sp1-dependent enhancers, although they showed promoter repression, which is a requirement for delineating enhancer function. In contrast, both Sp1-dependent promoters and enhancers were functional in two- to four-cell embryos. Furthermore, the same embryonic stem cell mRNA that provided the coactivator activity for Gal4:VP16-dependent enhancer function also provided Sp1-dependent enhancer function in oocytes. Therefore, the coactivator activity appears to be a requirement for general enhancer function. To determine whether the absence of enhancer function is a unique property of oocytes or a general property of other terminally differentiated cells, transcription was examined in terminally differentiated hNT neurons and their precursors, undifferentiated NT2 stem cells. The results showed that both cell types could utilize enhancers and promoters. Thus, in mammals, the lack of enhancer function appears to be unique to oocytes and fertilized eggs, suggesting that it provides a safeguard against premature activation of genes prior to zygotic gene expression during development.

Animals↗

PubMed2000

SOX9 enhances aggrecan gene promoter/enhancer activity and is up-regulated by retinoic acid in a cartilage-derived cell line, TC6.

SOX9 is a transcription factor that plays a key role in chondrogenesis. Aggrecan is one of the major structural components in cartilage; however, the molecular mechanism of aggrecan gene regulation has not yet been fully elucidated. TC6 is a clonal chondrocytic cell line derived from articular cartilage. The purpose of this study was to examine whether SOX9 modulates aggrecan gene expression and to further identify molecules that regulate Sox9 expression in TC6 cells. SOX9 overexpression in TC6 cells enhanced by approximately 3-fold the transcriptional activity of the AgCAT-8 construct containing 8-kilobase (kb) promoter/first exon/first intron fragments of the aggrecan gene. SOX9 enhancement of aggrecan promoter activity was lost when we deleted a 4.5-kb fragment from the 3'-end of the 8-kb fragment corresponding to the region including the first intron. In TC6 cells, SOX9 enhanced the transcriptional activity of a reporter construct containing the Sry/Sox consensus sequence >10-fold. SOX9 enhancement of aggrecan gene promoter activity and SOX9 transactivation through the Sry/Sox consensus sequence were not observed in osteoblastic osteosarcoma cells (ROS17/2.8), indicating the dependence on the cellular background. Northern blot analysis indicated that TC6 cells constitutively express Sox9 mRNA at relatively low levels. To examine regulation of Sox9 gene expression, we investigated the effects of calciotropic hormones and cytokines. Among these, retinoic acid (RA) specifically enhanced Sox9 mRNA expression in TC6 cells. The basal levels of Sox9 expression and its enhancement by RA were observed similarly at both permissive (33 degrees C) and nonpermissive (39 degrees C) temperatures. Furthermore, RA treatment enhanced the transcriptional activity of a reporter construct containing the Sry/Sox consensus sequence in TC6 cells. Moreover, RA treatment also enhanced the transcriptional activity of another reporter construct containing the enhancer region of the type II procollagen gene in TC6 cells. These observations indicate that SOX9 enhances aggrecan promoter activity and that its expression is up-regulated by RA in TC6 cells.

Aggrecans↗

PubMed2000

NF-kappa B activity is required for the deregulation of c-myc expression by the immunoglobulin heavy chain enhancer.

The c-myc gene is translocated to one of the immunoglobulin genes in Burkitt's lymphoma resulting in deregulated expression of c-myc. Several enhancers have been shown to be important for expression of the immunoglobulin heavy chain gene. Four enhancer regions (murine-hypersensitive sites (MHS) 1, 2, 3, and 4) located 3' of the murine immunoglobulin heavy chain gene play a role in activating expression of the translocated c-myc gene. The enhancer regions also result in a shift in transcriptional initiation from the P2 promoter to P1 that is characteristic of the translocated c-myc allele. We found that the most 3' enhancer region (MHS4) activated the c-myc promoter by 46-fold in the Raji Burkitt's lymphoma cell line, and it was the most active enhancer in these cells. The addition of enhancer regions MHS1,2 and 3 to MHS4 increased c-myc transcription by an additional 3-fold and resulted in the full promoter shift from P2 to P1. By deletion analysis of enhancer region MHS4, we located a region that was critical for the transcriptional activity of MHS4. Electrophoretic mobility shift assay analysis revealed that NF-kappaB/Rel family members bound to this region. Mutation of the NF-kappaB binding site abolished both the enhancer activity and the promoter shift activity of MHS4. An active NF-kappaB site was also identified in the human HS4 enhancer. Inhibition of c-myc promoter activity driven by the immunoglobulin enhancers was observed with expression of a super-repressor IkappaBalpha construct. These results indicate that the NF-kappaB/Rel transcription factors play an important role in the deregulation of the translocated c-myc gene in Burkitt's lymphoma and suggest that interference with NF-kappaB function may represent a new approach to the treatment of Burkitt's lymphoma.

Animals↗

PubMed2004

T-cell activation leads to poor activation of the HIV-1 clade E long terminal repeat and weak association of nuclear factor-kappaB and NFAT with its enhancer region.

The enhancer region in the human immunodeficiency virus type 1 (HIV-1) 5'-long terminal repeat (LTR) is very important for viral transcription. This promoter sequence binds both nuclear factor-kappaB and NFAT, two important modulators of HIV-1 gene expression. Previous studies have indicated that the enhancer regions of the different HIV-1 clade LTRs differ in their number of NF-kappaB-binding sites. In this study, we have compared the activation potential of the different HIV-1 clade and HIV-2 LTRs and assessed their interaction with NFAT and NF-kappaB. In T-cell lines and primary CD4(+) T-cells, the results showed that the HIV-1 clade E LTR (with a single NF-kappaB-binding site) was the weakest LTR regardless of the tested activators, whereas the HIV-2 LTR was the most responsive LTR. The clade E enhancer region was also demonstrated to be the weakest enhancer region in transfection experiments with luciferase reporter-based vectors. Electrophoretic mobility shift assays with extracts from activated CD4(+) T-cells indicated that, although NF-kappaB and NFAT bound all enhancers, HIV-1 clade E and HIV-2 LTR enhancers were poor binding targets for these two factors. Weak NFAT binding to clade E enhancers was also confirmed using NFAT1-expressing 293T cells in competition experiments. We have also shown the absence of interaction of NF-kappaB or NFAT with the third NF-kappaB repeat present in clade C. However, the clade C enhancer bound NFAT more efficiently than all other enhancer regions tested. Our results hence demonstrate for the first time that differences in the binding of NF-kappaB and NFAT to the enhancer regions could be responsible for some of the observed variation in HIV-1 clade LTR activation, whereas HIV-2 LTR activation seems mostly independent of these interactions.

Binding Sites↗

PubMed2005

Cdx binding determines the timing of enhancer activation in postnatal duodenum.

In mammalian intestine, adenosine deaminase (ADA) is expressed at high levels only along the villi of the duodenal epithelium. A duodenum-specific enhancer identified in the second intron of the human ADA gene controls this pattern of expression. This enhancer faithfully recapitulates this expression pattern in transgenic mice, when included in CAT reporter gene constructions. Multiple binding sites for PDX-1 and GATA factors were previously identified within the approximately 300-bp region that encompasses the enhancer. Mutation analyses demonstrated that binding of PDX-1 and of GATA-4 was absolutely essential for enhancer function. In the present study, we have identified additional enhancer binding sites for Cdx factors, for YY1, and for NFI family members. Detailed EMSA studies were used to confirm binding at these sites. This brings the number of confirmed binding sites within the enhancer to thirteen, with five different factors or family of factors contributing to the putative enhanceosome complex. Mutation analysis was utilized to examine the specific roles of the newly identified sites. Two sites were identified that bound both Cdx1 and Cdx2. Mutations were identified in these two sites that completely and specifically eliminated Cdx binding. In transgenic mice, these enhancer mutations dramatically changed the developmental timing of enhancer activation (delaying it by 2-3 weeks) without affecting other aspects of enhancer function. In the chromatin context of certain transgenic insertion sites, mutation of the two YY1 sites to specifically ablate binding caused a delay in enhancer activation similar to that observed with the Cdx mutations. No overt changes were observed from mutation of the NFI site.

Adenosine Deaminase↗

PubMed1996

Bifunctionality of the AcMNPV homologous region sequence (hr1): enhancer and ori functions have different sequence requirements.

The Autographa californica multinucleocapsid nuclear polyhedrosis virus (AcMNPV) homologous region sequence hr1 is a putative origin of replication (ori) sequence and can also function as a transcriptional enhancer for delayed-early genes. We demonstrate that this 750-bp sequence, carrying five 28-bp core palin-dromes, enhances expression from the very late polyhedrin promoter up to 11-fold in a classical enhancer fashion in transient expression assays. Enhancement is at the level of transcription, as evident from RNase protection assay analysis. It is mediated by an alpha-amanitin-insensitive RNA polymerase from the authentic polyhedrin promoter transcription start site and follows the temporal activation profile characteristic of the polyhedrin promoter. Three lines of evidence conclusively demonstrated that hr1 acts typically as an enhancer of polyhedrin gene transcription independent of its role as an ori: (i) linearized hr1-reporter plasmids, incapable of replicating in the host cell, could enhance transcription from the promoter; (ii) reporter plasmid copy number was not affected by the presence of aphidicolin during transfection; (iii) reporter plasmid DNA recovered from Sf9 cells was sensitive to Dpn I confirming its unreplicated state in the transfection regime followed by us. Molecular dissection of the hr1 sequence elements revealed that a core palindrome alone can function as an ori sequence whereas a palindrome along with flanking sequences is essential for the enhancer activity. Enhancement of luciferase expression from the polyhedrin promoter is a function of the number of core palindromes and flanking sequences. Our results demonstrate that hr1, which has several motifs for enhancer binding proteins and transcription factors, has a dual role associated with both DNA replication and transcriptional enhancement.

Animals↗

PubMed2004

An insulator blocks spreading of histone acetylation and interferes with RNA polymerase II transfer between an enhancer and gene.

We studied the mechanism by which an insulator interrupts enhancer signaling to a gene using stably replicated chromatin templates containing the human beta-globin locus control region HS2 enhancer and a target globin gene. The chicken beta-globin 5' HS4 (cHS4) insulator acted as a positional enhancer blocker, inhibiting promoter remodeling and transcription activation only when placed between the enhancer and gene. Enhancer blocking by cHS4 reduced histone hyperacetylation across a zone extending from the enhancer to the gene and inhibited recruitment of CBP and p300 to HS2. Enhancer blocking also led to accumulation of RNA polymerase II at HS2 and within cHS4, accompanied by its diminution at the gene promoter. The enhancer blocking effects were completely attributable to the CTCF binding site in cHS4. These findings provide experimental evidence for the involvement of spreading in establishment of a broad zone of histone modification by an enhancer, as well as for blocking by an insulator of the transfer of RNA polymerase II from an enhancer to a promoter.

Acetylation↗

PubMed1987

The SV40 enhancer can be dissected into multiple segments, each with a different cell type specificity.

The SV40 enhancer is known to be active in a wide variety of tissues and species. It contains a number of sequence motifs that can be bound by protein factors and whose integrity is essential for full enhancer activity. We have individually analyzed three synthetic oligonucleotides derived from sequences present within the SV40 enhancer: two oligonucleotides contain variants of the enhancer "core" sequence (designated corePVUII and coreC) and the third represents a region containing a decanucleotide homology to the immunoglobulin promoters/enhancers (designated SPHI). The oligonucleotides were multimerized and linked to a beta-globin test gene. Transcripts of the test gene were analyzed following transient expression in 10 cell lines representing a broad spectrum of tissues. We show that each of the three short segments can individually act as an enhancer when present in multiple copies. None of these enhancers is ubiquitously active; however, each shows activity in a distinctive subpopulation of cell lines. This cell type specificity is most remarkable in the case of the two oligonucleotide segments containing the core sequences. One of these is primarily active in CV-1 cells, whereas the other exhibits a cell type specificity identical to that of the entire enhancer, possibly identifying it as the most important sequence element within the native SV40 enhancer. Our data suggest that a particular cell type specificity is typical for individual enhancer segments, and that enhancers of differing specificity can be assembled from the individual sequence motifs by combining them in different patterns.

Animals↗

PubMed1988

Functional mapping of the human papillomavirus type 11 transcriptional enhancer and its interaction with the trans-acting E2 proteins.

The transcriptional enhancer sequences of the papillomaviruses are regulated by trans-acting factors encoded by the viral E2 open reading frame. We have performed detailed functional and physical analyses of the enhancer of the human papillomavirus type 11 (HPV-11). Using the chloramphenicol acetyltransferase (CAT) assay in transiently transfected monkey CV-1 cells, the enhancer region has been localized to a 270-bp tract immediately preceding the E6 open reading frame, and it consists of two functional components. The first is a constitutive enhancer containing sequences homologous to the GT-, Sph-, and P-motifs found in the SV40 and polyomavirus enhancers; others resemble the recognition sequence for CTF (NF-1), a factor which stimulates transcription of certain eukaryotic genes and replication of adenovirus DNA. The second component is an inducible enhancer with a consensus sequence ACCN6GGT responsive to the E2 protein encoded by papillomaviruses. Tandem copies of portions of the constitutive enhancer function as an E2-independent enhancer, whereas multiple copies of HPV-11 DNA restriction fragments or synthetic oligonucleotides containing the E2-responsive sequence (E2-RS) act as an enhancer in the presence of the E2 protein encoded by HPV-1, HPV-11, or bovine papillomavirus type 1 (BPV-1). The inducible activity is lost when mutations are introduced into the E2-RS or when a mutant palindromic sequence is substituted. We have also expressed the E2 proteins of HPV-1, HPV-11, and BPV-1 in Escherichia coli and studied their physical interactions with the E2-responsive sequence in vitro. Filter-binding analyses with crude Escherichia coli lysates show that the E2 proteins bind to the E2-RS, but not to mutated motifs, with an affinity proportional to the copy number. These E2 proteins have been purified to near-homogeneity by sequence-specific DNA affinity chromatography using the synthetic E2-RS as a ligand. The purified proteins protect a DNA segment containing the E2-RS and several flanking nucleotides in pancreatic DNase I footprinting analyses. Based on these results, we conclude that E2 proteins activate the enhancer by binding directly to the E2-RS and interacting with other transcriptional factors and that the sequence ACCN6GGT is both necessary and sufficient for the E2 protein binding in vitro and for activation of RNA transcription in vivo.

Chromosome Deletion↗

PubMed2005

Recognition performance and perceived quality of video enhanced for the visually impaired.

Subjects with central field loss (CFL) individually selected enhancement parameters to improve visibility of static video images. The effect of enhancement on performance and on perceived quality of motion video was assessed. Performance, e.g. recognition of visual details, was assessed by having subjects answer questions regarding visual information contained in the video motion segments that were enhanced using the individually-selected parameters. Enhancement did not improve subject performance on questions about video content. This result might be due to a ceiling effect limitation of the performance assessment method. In a second procedure, subjects' continuous perceptions of quality (using an adjective-based rating scale) were made while the enhancement parameters were abruptly switched among multiple values; these included the individually-selected enhancements, as well as unenhanced, over-enhanced, and degraded segments. The results indicate that adaptive enhancement (individually-tuned using a static image) adds significantly to perceived image quality when viewing motion video. Subjects who selected stronger contrast enhancement also perceived the enhancement to provide a larger benefit in image quality.

Contrast Sensitivity↗

PubMed1987

Effects of position and orientation of the 72-base-pair-repeat transcriptional enhancer on replication from the simian virus 40 core origin.

A number of recent studies have reported that in papovaviruses such as simian virus 40 (SV40) and polyomavirus, the replication of the viral DNA in vivo is activated by the viral transcriptional enhancer or promoter sequences. Both viral and cellular transcriptional enhancers are well known for their ability to activate transcription in a position- and orientation-independent manner. In the present study, we investigated the effect of the position and orientation of the SV40 72-base-pair (bp) repeat enhancer on its replication activation function. We constructed plasmids containing one copy each of the SV40 core origin and enhancer placed in either order and orientation and at different distances from each other. We assayed the replication efficiencies of these plasmids in the presence of an internal control plasmid in COS-1 monkey kidney cells producing the SV40 T antigen required for replication. We found that the 72-bp repeat was capable of activating replication equally well in either orientation when placed 8 or 9 bp from the core origin. The activation of replication was totally abolished, and replication efficiencies in most instances were found to be lower than that obtained with the core origin alone, when the 72-bp repeat was separated from the core origin by distances of 99 bp or more. This was in direct contrast to the situation with polyomavirus, in which activation of replication by the homologous enhancer or by the SV40 72-bp repeat enhancer is known to be position independent. We also found that when the SV40 core origin and the 72-bp repeat enhancer were adjacent to each other, efficient activation of replication was obtained only if the end of the core origin containing the 17-bp A + T block was linked with the enhancer. In the other orientation of the core origin, activation of replication was either diminished or abolished. Hypotheses such as alteration of chromatin structure by the enhancer and interaction between trans-acting factors binding to the enhancer and the core origin mediating the activation effect are discussed.

Animals↗