SEARCH · PubMed Health

Results for “regulatory element transcripts”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,513 records · Page 84Linked to original sources

PubMed1992

Identification of a cis-regulatory element mediating somatostatin inhibition of epidermal growth factor-stimulated gastrin gene transcription.

Antral gastrin secretion and gene expression is inhibited by the paracrine release of somatostatin from antral D cells. Transforming growth factor-alpha and epidermal growth factor (EGF) stimulate gastrin reporter gene constructs when transfected into pituitary GH4 cells. Somatostatin inhibits EGF stimulation of gastrin gene expression, which is in part mediated at the level of transcriptional regulation as somatostatin inhibits EGF stimulation of gastrin reporter gene constructs. Somatostatin inhibition was abolished by pertussis toxin, indicating somatostatin inhibits transcription through the inhibitory G protein Gi. Somatostatin inhibition was unaffected by vanadate and okadaic acid, implying this inhibitory pathway is mediated neither through phosphotyrosine phosphatases nor serine/threonine phosphatases, respectively. Gastrin reporter genes containing 82 base pairs of the 5'-flanking DNA were sufficient to confer both EGF responsiveness and inhibition by somatostatin in GH4 cells. However, transcription of a gastrin reporter gene construct containing only the EGF response element (GGGGCGGGGTGGGGGG), located at -68 to -53, was stimulated by EGF but was not inhibited by somatostatin. Thus, somatostatin inhibits EGF-stimulated gastrin gene transcription by a mechanism other than by interfering with cell signals elicited by the EGF receptor. Since the 82 GASCAT is inhibited by somatostatin, this result also implies that sequences adjacent to the EGF response element contain a cis-regulatory element mediating transcriptional inhibition by somatostatin. This cis-element was located using gastrin reporter genes comprising sequential segments of the human gastrin promoter sequence from the transcriptional start site to -82 in the 5'-flanking DNA. Gastrin oligonucleotide constructs lacking the D oligonucleotide (gatcCATATGGCAGGGTA), located at -82 to -69 in the 5'-flanking DNA, were not inhibited by somatostatin, indicating that a somatostatin inhibitory cis-element is located between -82 and -69 in the 5'-flanking DNA of the human gastrin promoter.

Animals↗

PubMed2004

Transcriptional regulation of human SREBP-1c (sterol-regulatory-element-binding protein-1c): a key regulator of lipogenesis.

Sterol-regulatory-element-binding protein 1c (SREBP-1c) is one member of the family of transcription factors that stimulate sterol and fatty-acid biosynthesis in animal cells. Human SREBP-1c, mapped to chromosome 17p11.2, is expressed in liver, intestine, skeletal muscle and adipocytes. A section of genomic sequence from a chromosome 17 library, thought to contain the SREBP-1c promoter, was cloned. Putative transcription-factor-binding sites and a potential transcriptional start site were identified using the Genomatix Suite of sequence analysis tools (MatInspector). Sequence analysis showed the human promoter to be 42% identical with the previously published mouse sequence. Two novel transcription-factor-binding sites were identified: those for PDX-1 (pancreatic-duodenal homoeobox-1) and HNF-4 (hepatic nuclear factor-4). Co-transfection experiments with overexpression plasmids for PDX-1 and HNF-4 suggested that both factors stimulate SREBP-1c gene expression, although further work is required to ascertain their mechanisms of action.

Animals↗

PubMed2004

Transcriptional regulation of antigen presentation.

MHC class I and class II molecules play essential roles in the adaptive immune response by virtue of their ability to present peptides to T lymphocytes. Given their central role in adaptive immunity, the genes encoding these peptide-presenting molecules are regulated in a tight fashion to meet with local requirements for an adequate immune response. In contrast to MHC class I gene products, which are expressed on almost all nucleated cells, constitutive expression of MHC class II molecules is found only in specialized antigen-presenting cells of the immune system. Expression of both classes of MHC molecules can be induced by immune regulators and upon cell activation. A set of conserved cis-acting regulatory promoter elements mediate the transcription of MHC class I and beta2-microglobulin genes. Of these regulatory elements, the promoters of MHC class II and accessory genes also have the SXY module. The MHC class II transactivator (CIITA) is essential for the activation of MHC class II promoters, and it functions through protein-protein interactions with regulatory factors bound to the SXY module. Given the central role of CIITA in these regulatory processes, it is of interest to identify the DNA-binding factors and co-activators that assemble on CIITA promoters in a cell-type-specific fashion. Accordingly, recent studies include investigations into chromatin remodeling and epigenetic control mechanisms that modulate cell-type-specific transcriptional regulation of genes involved in antigen presentation.

Animals↗

PubMed1997

Optimization of the human factor VIII complementary DNA expression plasmid for gene therapy of hemophilia A.

While the gene delivery vehicle is critical for the efficacy of human factor VIII gene therapy, optimization of the potency and duration of the factor VIII gene that is delivered is equally important in light of the poor transcription and translation characteristics of this gene. We discuss here a systematic approach to optimization of factor VIII complementary DNA expression by analysis of specific elements engineered into the transcription unit and other positions in the expression plasmid. Within the transcription unit we have engineered different 5' and 3' sequence modifications and tested them for factor VIII expression in human liver cells. These changes incorporate liver-specific promoter and enhancer sequences and regulatory elements affecting RNA export. Specifically, the thyroid hormone-binding globulin promoter and alpha 1 microglobulin/bikunin enhancer were tested and a synthetic 5' intron was compared to a 3' post-transcriptional regulatory element on factor VIII expression levels. For translation optimization, a leader sequence was designed to be of optimum length, have no RNA secondary structure and contain the optimal translation initiation sequence. Finally, we discuss areas for plasmid optimization, which include removal of near-consensus splicing sequences, the inclusion of strong transcription termination elements and the use of autonomous replicating plasmid sequences for episomal maintenance and enhanced plasmid retention for duration of gene expression.

Carcinoma, Hepatocellular↗

PubMed2002

Analysis of the promoter region of human mimecan gene.

Mimecan is a small leucine-rich proteoglycan (SLRP) that may play an important role in the regulation of cellular growth as illustrated by ability of growth factors and cytokines to modulate its expression and by recent demonstration that bovine mimecan is transcriptionally activated by p53 through a conserved intronic recognition site. To investigate transcriptional regulation of human mimecan, the upstream region and the first intron of this gene were cloned and analyzed. Within a 296-bp upstream region required for basal gene expression, there are three initiator (Inr) elements, an E-box and Oct-1, metal response element (MRE), and NF-kappa B recognition sites. Upstream stimulatory factor (USF)-1, Oct-1 and MRE-binding proteins were identified as proteins that bind to these regulatory elements and support transcription of mimecan in MG-63 cells. The first intron of human mimecan contains enhancer and silencer elements. Reporter gene transfections demonstrated that cooperation of upstream region and intronic enhancer elements are required for maximal gene expression in both p53-deficient and wild-type p53-expressing cells. Within the footprinted intronic enhancer region an interferon-stimulated response element (ISRE) is present. Using electrophoretic mobility shift assay (EMSA), interferon regulatory factor (IRF)-1 was identified as a protein that binds to this region in MG-63 but not in U-937 cells. In vitro translated IRF-1 also was shown to bind to this ISRE. These results demonstrate that the first intron of human mimecan gene carries important regulatory elements, including p53 DNA-binding site and ISRE, and should promote a better understanding of molecular bases for cell type-specific regulation of mimecan transcription.

5' Flanking Region↗

PubMed2002

Functionality of two new polymorphisms in the human renin gene enhancer region.

BACKGROUND: The production of renin, which catalyses the rate-limiting step of the renin-angiotensin system, is strongly stimulated by a 225 bp enhancer element in the distal region of the promoter of the human gene (-5777 to -5552). OBJECTIVE: To demonstrate the major role played by this enhancer in decoy experiments, to identify variants in this region, and to determine their effects on renin gene transcription. METHODS AND RESULTS: We used this element as a decoy for transcription factors in human choriodecidual cells. The activity of the renin gene promoter was inhibited by 95% in the presence of this 225 bp enhancer element. This confirmation of the key role of this element suggested that changes in this region would be likely to affect renin gene expression. We therefore sequenced 70 genomic DNAs to identify variations in this region. We identified two new single nucleotide polymorphisms (SNPs) downstream from the 225 bp enhancer element at positions -5434 and -5312. We transfected choriodecidual cells with the four variants and found that a 592 bp region (-5870 to -5312) including the 225 bp element and the two SNPs had stronger enhancer activity than the 225 bp element alone, and that levels of transcription were 45% greater with the -5312T variant than with the -5312C variant, whereas none of the -5434 variants had an effect on renin transcription. Cis-regulatory elements close to the -5312 variant were identified in gel mobility shift assays on the basis of specific interactions between human choriodecidual cell nuclear extracts and an oligonucleotide including this polymorphism. CONCLUSION: This study demonstrates that the human renin enhancer not only comprises the 225 bp element, but also extends to the region containing the -5312 SNP.

Amino Acid Sequence↗

PubMed1999

A novel negative cis-regulatory element on the hepatitis B virus S-(+)-strand.

Hepatitis B virus (HBV) has a double-stranded DNA genome. The minus-strand contains coding regions for all known HBV proteins and most of the cis-regulatory elements. Little is known about transcription from the S-(+)-strand and its regulation. Thus, the presence of regulatory elements located on the S-(+)-strand was investigated by inserting nt 1038-1783 of HBV in both orientations between the human cytomegalovirus (HCMV) promoter and a luciferase gene. Transfection experiments revealed that the plasmid containing this HBV DNA fragment in an orientation allowing expression from the S-(+)-strand (antisense) led to inhibition of luciferase gene expression compared to the plasmid containing this sequence in an orientation that allows gene expression from the L-(-)-strand (sense). Deletion analyses delimit the sequence essential for the inhibitory effect to a 150 bp region that also carries part of the enhancerII/core promoter complex. However, the possible influence of this regulatory element has been excluded in various experiments. The repressing HBV sequence acts in an orientation- and position-dependent manner; no inhibition was observed when this DNA element was inserted upstream of the HCMV promoter or downstream of the luciferase gene. Northern blot analyses revealed reduced luciferase mRNA steady-state levels in cells transfected with constructs containing the essential HBV sequence in antisense orientation compared to plasmids containing this sequence in sense orientation. Since nuclear run-on experiments showed similar transcription initiation rates with these plasmids, the diminished luciferase mRNA steady-state levels must be due to altered stabilities, suggesting that nt 1783-1638 of HBV encode an RNA-destabilizing element.

DNA, Single-Stranded↗

PubMed2001

Characterization of the promoter region of the viral interferon regulatory factor encoded by Kaposi's sarcoma-associated herpesvirus.

Viral interferon regulatory factor (vIRF) encoded by Kaposi's sarcoma-associated herpesvirus (KSHV) inhibits the expression of interferon-responsive genes, causes cellular transformation and transactivates KSHV genes. In the present study, we characterized the mRNA expression pattern of the vIRF gene and its promoter. A vIRF transcript of 1.7 kb in size was detected in low level in uninduced KSHV-infected cells and its expression was inducible by 12-O-tetradecanoylphorbol-13-acetate (TPA), sensitive to cycloheximide and resistant to phosphonoacetic acid. The transcription start site was mapped to 79 nt upstream of the ATG initiation site by 5'-RACE. Mutagenesis analysis identified a region between -56 and the transcription start site (+1) as the minimal promoter region that contains a functional TATA box at -27. A region between -337 and -125 contains a repressor domain negated by sequence from -991 to -499 in BCBL-1 cells, a region which was also identified to be responsive to TPA induction. These results demonstrate vIRF as a KSHV early gene, identify its promoter and define the promoter regions that contain regulatory elements controlling vIRF transcription.

Base Sequence↗

PubMed2000

Transcriptional control elements of the rat thymidylate synthase promoter: evolutionary conservation of regulatory features.

The sequence elements that are important for the transcription and regulation of the rat thymidylate synthase (TS) gene were analyzed. The rat TS promoter lacks a TATA box and directs transcriptional initiation at multiple sites between 60 and 20 nt upstream of the AUG translational start codon. Promoter deletion analyses showed that the region between -100 and -42 nt relative to the AUG codon was both necessary and sufficient for high level promoter activity and was designated the essential promoter region. The essential region also had bidirectional promoter activity. Site-directed mutagenesis revealed that four elements were especially important for promoter activity. These include Ets motifs at -85 and -50, an Sp1 motif at -80, and an LSF motif that overlapped the upstream Ets and Sp1 motifs. Inactivation of E2F motifs that are upstream and downstream of the essential promoter region had no measurable effect on promoter activity in transient transfection assays. The rat TS promoter region directed S-phase-specific expression of a stably transfected minigene if a spliceable intron was included in the transcribed region. When the intron was deleted or the E2F motifs were inactivated, expression of the minigene changed very little during the G1 to S transition.

Animals↗

PubMed1986

Delimitation and characterization of cis-acting DNA sequences required for the regulated expression and transcriptional control of the chicken skeletal alpha-actin gene.

We have previously observed that DNA sequences within the 5'-flanking region of the chicken skeletal alpha-actin gene harbor a cis-acting regulatory element that influences cell type and developmental stage-specific expression (J. M. Grichnik, D. J. Bergsma, and R. J. Schwartz, Nucleic Acids Res 14:1683-1701, 1986). In this report we have constructed unidirectional 5'-deletion and region-specific deletion-insertion mutations of the chicken skeletal alpha-actin upstream region and inserted these into the chloramphenicol acetyltransferase expression vector pSV0CAT. These constructions were used to locate DNA sequences that are required for developmental modulation of expression when transfected into differentiating myoblasts. With this assay we have delimited the 5' boundary of a cis-acting regulatory element to ca. 200 base pairs upstream of the mRNA cap site. In addition, we have preliminarily identified DNA sequences that may be important subcomponents within this element. A second major focus of this study was to identify those DNA signals within the regulatory element that control transcription. Toward this end, the expression phenotypes of progressive 5'-deletion and deletion-insertion mutants of the 5'-flanking region of the chicken skeletal alpha-actin gene were assayed in microinjected Xenopus laevis oocytes. These experiments defined a cis-acting transcriptional control region having a 5' border 107 base pairs preceding the alpha-actin RNA cap site. Proximal and distal functionally important regions of DNA were identified within this element. These DNA signals included within their DNA sequences the "CCAAT" and "TATA" box homologies.

Actins↗

PubMed1989

The gradient morphogen bicoid is a concentration-dependent transcriptional activator.

The bicoid (bcd) protein is expressed in an anteroposterior gradient in early Drosophila embryos and controls the zygotic activation of the segmentation gene hunchback (hb) in a broad but precisely bounded anterior domain. Here we show that the hb gene contains multiple regulatory elements that mediate transcriptional activation in response to bcd protein. Further, we demonstrate that the resulting patterns of expression in vivo depend critically on both the bcd gradient profile and the number and quality of these hb elements. Finally, we show that these same elements mediate bcd-dependent transcriptional activation in yeast and that this interaction requires distinct DNA binding and activating regions in the bcd protein. Our results argue that bcd protein normally binds and activates the hb gene in a concentration-dependent fashion, thereby allowing the gradient of bcd protein to dictate where the hb gene is initially turned on in early embryos. They also suggest that the bcd gradient has the instructive capacity to activate other subordinate control genes by the same mechanism, each in a distinct spatial domain according to its affinity for bcd protein.

Animals↗

PubMed1996

PEA3 transactivates vimentin promoter in mammary epithelial and tumor cells.

We have used differential display RT-PCR method to detect the genes specifically activated or repressed between mammary tumor and normal mammary epithelial cells. One of the genes identified is vimentin. The vimentin gene is abundantly expressed in both human and mouse mammary tumor cells and its expression decreased dramatically in normal mammary epithelial cells. The expression of vimentin gene correlates with the expression of transcription factor PEA3. Since the promoters of human and mouse vimentin genes contain one PEA3 binding site we investigated the ability of PEA3 to transactivate the vimentin promoter in mouse mammary epithelial cell CLS1, mouse mammary tumor MMT and human mammary tumor cell lines MCF7 and MDA231. Our results suggest that PEA3 specifically transactivates vimentin promoter through PEA3 site. Among members of the ETS transcription factor family only Erg showed ability to transactivate vimentin promoter besides PEA3. Our results also suggest that NFkB site on the vimentin promoter may act as a positive regulatory element for the transcription of vimentin. In metastatic mammary tumors derived from mice carrying the polyoma middle T or neu transgene, PEA3 is overexpressed and vimentin has been shown to play a key role in the motility of cells. Our results suggest that one of the roles of PEA3 in mammary tumor is to participate the activation of vimentin gene whose gene product in turn contributes to the metastatic potential of mammary tumors.

Animals↗

PubMed2001

Ku represses the HIV-1 transcription: identification of a putative Ku binding site homologous to the mouse mammary tumor virus NRE1 sequence in the HIV-1 long terminal repeat.

Ku has been implicated in nuclear processes, including DNA break repair, transcription, V(D)J recombination, and telomere maintenance. Its mode of action involves two distinct mechanisms: one in which a nonspecific binding occurs to DNA ends and a second that involves a specific binding to negative regulatory elements involved in transcription repression. Such elements were identified in mouse mammary tumor virus and human T cell leukemia virus retroviruses. The purpose of this study was to investigate a role for Ku in the regulation of human immunodeficiency virus (HIV)-1 transcription. First, HIV-1 LTR activity was studied in CHO-K1 cells and in CH0-derived xrs-6 cells, which are devoid of Ku80. LTR-driven expression of a reporter gene was significantly increased in xrs-6 cells. This enhancement was suppressed after re-expression of Ku80. Second, transcription of HIV-1 was followed in U1 human cells that were depleted in Ku by using a Ku80 antisense RNA. Ku depletion led to a increase of both HIV-1 mRNA synthesis and viral production compared with the parent cells. These results demonstrate that Ku acts as a transcriptional repressor of HIV-1 expression. Finally, a putative Ku-specific binding site was identified within the negative regulatory region of the HIV-1 long terminal repeat, which may account for this repression of transcription.

3T3 Cells↗

PubMed1989

Multiple protein-DNA interactions within the human interferon-beta regulatory element.

High efficiency nuclear protein extracts were prepared from uninduced and recombinant interferon (IFN-alpha 2-primed Sendai virus-induced HeLa S3 cells and analyzed for DNA binding proteins specific for the human interferon-beta regulatory element (IRE). Analysis of protein-DNA interactions by a gel electrophoresis DNA binding assay resolved three complexes (designated A, B, and C) specific for the IRE probe (-79 to -36) in uninduced and induced cells. Competition studies using greater than a 100-fold molar excess of unlabeled DNA fragments representing different IFN-beta promoter sequences localized the DNA binding domain to the region -79 to -64 (P1 probe), a region previously shown to be essential for virus-inducible gene expression. Other adjacent IFN-beta segments including the negative regulatory element (-65 to -30) as well as the SV40 enhancer, c-fos serum-responsive element, and IFN-alpha 1 promoter fragment (-131 to -71) were unable to compete for the IRE binding protein. The 16-base pair enhancer core (P1 probe) specifically bound similar amounts of protein from uninduced and induced extracts; a synthetic tetrahexamer, AAGTGA, competed efficiently for the binding to the P1 region. Competition studies indicated that adjacent upstream IFN-beta DNA sequences -94 to -78 (P5) also contained a sequence motif capable of binding the P1 protein. In vitro transcription of the IFN-beta template in the HeLa nuclear extracts was partially inhibited when increasing amounts of competitor IRE fragment were added to the reaction. These results demonstrate that multiple DNA sequence motifs within the IFN-beta regulatory element interact to bind transcription regulatory proteins which are present in normal and virus-infected HeLa cells.

Base Sequence↗

PubMed2003

CONREAL: conserved regulatory elements anchored alignment algorithm for identification of transcription factor binding sites by phylogenetic footprinting.

Prediction of transcription-factor target sites in promoters remains difficult due to the short length and degeneracy of the target sequences. Although the use of orthologous sequences and phylogenetic footprinting approaches may help in the recognition of conserved and potentially functional sequences, correct alignment of the short transcription-factor binding sites can be problematic for established algorithms, especially when aligning more divergent species. Here, we report a novel phylogenetic footprinting approach, CONREAL, that uses biologically relevant information, that is, potential transcription-factor binding sites as represented by positional weight matrices, to establish anchors between orthologous sequences and to guide promoter sequence alignment. Comparison of the performance of CONREAL with the global alignment programs LAGAN and AVID using a reference data set, shows that CONREAL performs equally well for closely related species like rodents and human, and has a clear added value for aligning promoter elements of more divergent species like human and fish, as it identifies conserved transcription-factor binding sites that are not found by other methods. CONREAL is accessible via a Web interface at http://conreal.niob.knaw.nl/.

Algorithms↗

PubMed1991

Activity and enhancer binding factors for BK virus regulatory elements in differentiating embryonal carcinoma cells.

We have studied cell type specificity of expression of the human papovavirus BK regulatory elements in undifferentiated and differentiated embryonal carcinoma (EC) cells as a model system. While the activity of the regulatory elements of this virus was marginal in undifferentiated cells, differentiation by retinoic acid and DMSO resulted in a dramatic increase in the activity. To correlate in vivo activity of the regulatory elements with interaction with cellular transcription factors, we performed DNase I footprinting experiments. A GC-rich region was protected in both undifferentiated and differentiated cells. An additional four protected sites were detected in retinoic acid-differentiated cells and at least one of these additional sites was weakly protected in DMSO-differentiated cells. The sequences of the differentiated cell type-specific protected regions showed homology to a nuclear factor 1 (NF-1) binding motif and to a muscle creatine kinase gene enhancer motif. The intensity, competition, and pattern of protection of these sites were different in the two differentiated cell types, suggesting the involvement of different transcription factors regulating the activity of BKV regulatory elements in the two cell types.

BK Virus↗

PubMed1999

Independent promoters regulate the expression of two amino terminally distinct forms of latent transforming growth factor-beta binding protein-1 (LTBP-1) in a cell type-specific manner.

Latent transforming growth factor-beta (TGF-beta)-binding proteins (LTBPs) are components of the extracellular matrix and large latent TGF-beta complexes are secreted by various cells. Human LTBP-1 is known to exist in different forms. LTBP-1L (long) has an amino-terminal extension, which is not found in the smaller LTBP-1S isoform. To study the formation and transcriptional regulation of LTBP-1S and LTBP-1L isoforms, we determined the nucleotide sequences of their 5'-flanking regions. The upstream regions of both isoforms are devoid of TATA boxes but contain other putative binding sites for several transcription factors. Genomic sequencing revealed that LTBP-1L transcript is alternatively spliced to an internal splice acceptor inside exon 1 of LTBP-1S and thus defined the genomic organization of the isoforms. Reporter gene analysis of upstream regions indicated the presence of independent, functional promoters, which regulate the transcription of the isoforms by cell-specific manner. Deletion analyses of the promoter regions revealed specific elements modulating their basal and cell type-specific expression. In SV-40 virus-transformed WI-38 lung fibroblasts a regulatory element repressed the transcription of LTBP-1S by a cell-specific manner. In amniotic epithelial cells, transcription of the LTBP-1S reporter gene construct was down-regulated by a distal upstream element. mRNA levels of the isoforms of LTBP-1 were stimulated in response to TGF-beta1 in WI-38 cells. However, since TGF-beta1 failed to stimulate the transcription of LTBP-1 reporter gene constructs, TGF-beta1 may mediate the induction of the isoforms by post-transcriptional mechanisms. Chromosomal localization of the LTBP-1 gene was refined to 2p22-24.

Base Sequence↗

PubMed1998

The DNA puff gene BhC4-1 of Bradysia hygida is specifically transcribed in early prepupal salivary glands of Drosophila melanogaster.

The BhC4-1 gene of the sciarid Bradysia hygida is located at DNA puff C4 and is amplified and actively transcribed in the salivary gland at the end of the last larval instar. We show here that a 3.6 kb fragment from the upstream region of the BhC4-1 gene is able to drive transcription in transgenic Drosophila specifically in prepupal salivary gland in a temporally regulated manner. The mRNA is present in maximal amounts in prepupae +3 h; in prepupae +9 h the levels of BhC4-1 mRNA decline, and it is no longer detected in pupae +24 h. Taken together these results suggest that most, if not all, of the key promoter regulatory elements were included in the DNA fragments employed to transform Drosophila. Moreover, strong expression of the transgenes implies conservation of the regulatory elements involved, since Drosophila transcription factors appear to recognize B. hygida regulatory DNA sequences. Quantitative Southern blot hybridization indicates that the sequences from DNA puff C4 are not amplified at detectable levels in salivary glands of transgenic prepupae when the BhC4-1 gene is transcribed. Transcription of a DNA puff in the absence of amplification indicates that the induction of these processes involves distinct mechanisms.

Animals↗