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PubMed1992

The role of the stages of initiation and promotion in phenotypic diversity during hepatocarcinogenesis in the rat.

Differences in the distribution of phenotypic alterations in initiated and promoted cell populations reflect both the dose and the action of the specific initiating agent, as well as the mechanism of action of the promoting agent. The use of multiple phenotypic markers to characterize AHF should allow further experimentation on the characteristics of promoting agents in hepatocarcinogenesis, especially their ability to promote separate populations of initiated cells, and on those characteristics of initiated cells that enable certain ones to survive and multiply in the specific environment provided by a promoting agent. Studies of promoting agents with differing mechanisms of action should further allow questions of reversibility, substitution and additivity of the actions of promoting agents to be addressed. The possibility that individual promoting agents do not enhance the growth of the entire population of initiated cells indicates that study of combinations of promoting agents is an important future direction of research. Therefore, information on the characteristics of promoting agents, singly and in combination, is necessary to assess more accurately the contribution of promoting agents to the carcinogenic risk for humans distinct from the effects of initiating agents and complete carcinogens.

Animals↗
PubMed1994

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is expressed in mouse skin in response to tumor-promoting agents and modulates dermal inflammation and epidermal dark cell numbers.

In mouse dorsal skin multistage carcinogenesis models, tumor promotion can be mediated by chemical agents, but also by wounding or abrasion of the epidermis, suggesting that endogenous growth factors mediate this process. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is one such factor that has been reported to be produced by keratinocytes in vitro, and has been suggested both to stimulate keratinocyte proliferation, and also to be a chemoattractant for neutrophils and macrophages. In this study we examined the expression and function of GM-CSF in mouse skin following the application of tumor-promoting agents. Both single and multiple applications of 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in accumulation of GM-CSF mRNA in the epidermis. Various phorbol and non-phorbol ester tumor promoters were found to induce increases in epidermal GM-CSF mRNA levels commensurate with their relative tumor promoting capabilities. Fluocinolone acetonide (FA) and tosyl phenylalanine chloromethyl ketone (TPCK), inhibitors of tumor promotion, inhibited tumor promoter-mediated GM-CSF accumulation, whereas all-trans-retinoic acid (RA) enhanced the TPA-induced increase. The retinoic acid analogue RO-109359 which, unlike RA, does not have tumor promoting activity per se, inhibited the TPA-induced increase in epidermal GM-CSF mRNA levels. When an antibody specific to GM-CSF was administered prior to TPA, the promoter-induced dermal inflammation and increase in epidermal dark cell number were reduced, yet promoter-induced epidermal hyperplasia was not. These findings implied that elevation of GM-CSF levels plays an important role in chemically-mediated mouse skin tumor promotion and principally via effects on promoter-induced inflammation and increased epidermal dark cell number.

Animals↗
PubMed2005

Comprehensive analysis of transcriptional promoter structure and function in 1% of the human genome.

Transcriptional promoters comprise one of many classes of eukaryotic transcriptional regulatory elements. Identification and characterization of these elements are vital to understanding the complex network of human gene regulation. Using full-length cDNA sequences to identify transcription start sites (TSS), we predicted more than 900 putative human transcriptional promoters in the ENCODE regions, representing a comprehensive sampling of promoters in 1% of the genome. We identified 387 fragments that function as promoters in at least one of 16 cell lines by measuring promoter activity in high-throughput transient transfection reporter assays. These positive functional results demonstrate widespread use of alternative promoters. We show a strong correlation between promoter activity and the corresponding endogenous RNA transcript levels, providing the first experimental quantitative estimate of promoter contribution to gene regulation. Finally, we identified functional regions within a randomly selected subset of 45 promoters using deletion analyses. These experiments showed that, on average, the sequence -300 to -50 bp of the TSS positively contributes to core promoter activity. Interestingly, putative negative elements were identified -1000 to -500 bp upstream of the TSS for 55% of genes tested. These data provide the largest and most comprehensive view of promoter function in the human genome.

Gene Expression Regulation↗
PubMed2004

Evaluation of tissue specificity and expression strength of rice seed component gene promoters in transgenic rice.

Using stable transgenic rice plants, the promoters of 15 genes expressed in rice seed were analysed for their spatial and temporal expression pattern and their potential to promote the expression of recombinant proteins in seeds. The 15 genes included 10 seed storage protein genes and five genes for enzymes involved in carbohydrate and nitrogen metabolism. The promoters for the glutelins and the 13 kDa and 16 kDa prolamins directed endosperm-specific expression, especially in the outer portion (peripheral region) of the endosperm, whilst the embryo globulin and 18 kDa oleosin promoters directed expression in the embryo and aleurone layer. Fusion of the GUS gene to the 26 kDa globulin promoter resulted in expression in the inner starchy endosperm tissue. It should be noted that the 10 kDa prolamin gene was the only one tested that required both the 5' and 3' flanking regions for intrinsic endosperm-specific expression. The promoters from the pyruvate orthophosphate dikinase (PPDK) and ADP-glucose pyrophosphorylase (AGPase) small subunit genes were active not only in the seed, but also in the phloem of vegetative tissues. Within the seed, the expression from these two promoters differed in that the PPDK gene was only expressed in the endosperm, whereas the AGPase small subunit gene was expressed throughout the seed. The GUS reporter gene fused to the alanine aminotransferase (AlaAT) promoter was expressed in the inner portion of the starchy endosperm, whilst the starch branching enzyme (SBE1) and the glutamate synthase (GOGAT) genes were mainly expressed in the scutellum (between the endosperm and embryo). When promoter activities were examined during seed maturation, the glutelin GluB-4, 26 kDa globulin and 10 kDa and 16 kDa prolamin promoters exhibited much higher activities than the others. The seed promoters analysed here exhibited a wide variety of activities and expression patterns, thus providing many choices suitable for various applications in plant biotechnology.

Journal Article↗
PubMed1983

Transfer of sensitivity to tumor promoters by transfection of DNA from sensitive into insensitive mouse JB6 epidermal cells.

Sensitivity to promotion of transformation by tumor promoters in mouse epidermal JB6 cells appears to have a genetic basis since the phenotypes of both promotable and nonpromotable JB6 cells derived from a common parent line are stable. Hybridization of promotable (P(+)) and nonpromotable (P(-)) cells previously indicated that promotability appears to behave as a dominant trait. These results suggest that it should be possible to find DNA sequences which specify sensitivity to promotion of anchorage independence by 12-o-tetradecanoyl-phorbol-13-acetate (TPA). Cellular DNA isolated from one of two P(+) lines, JB6 Cl 41 or JB6 Cl 22, was CaPO(4) precipitated and used to transfect the P(-) cell line JB6 Cl 30. At 7 days posttransfection, the cells were suspended in agar with or without TPA at 1.6 x 10(-8) M and assayed 10 days later for TPA-dependent colony formation. Untreated or Cl 30 DNA-treated P(-) JB6 Cl 30 cells yielded 40 to 50 colonies per 10(5) cells. In contrast, transfection of Cl 30 cells with "P(+) DNA" derived from either Cl 41 or Cl 22 yielded 200 to 500 TPA-induced colonies per 10(5) cells, or a five- to eightfold enhancement of promotability. The enhanced promotability obtained after transfection with P(+) DNA was stable, as judged by the retention of promotability for at least eight passages in cell lines derived from TPA-induced agar colonies. Other transfectants showed irreversible transformation by TPA, as observed in the parental P(+) lines. When NIH 3T3 cells instead of the putative preneoplastic JB6 Cl 30 cells were used as recipients for transfection of P(+) DNA, no evidence for acquisition of promotability was obtained. P(-) JB6 Cl 25, like Cl 30, also permitted expression of transfected P(+) DNA. These results suggest that sensitivity to phorbol ester promotion of transformation in JB6 cells is determined by DNA sequence(s) present in the P(+) DNA and requires recipient cells of the appropriate phenotype for expression.

Animals↗
PubMed1991

A comparative study of the promotion of tissue plasminogen activator and pro-urokinase-induced plasminogen activation by fragments D and E-2 of fibrin.

Plasmin generation by equimolar concentrations of tissue plasminogen activator (t-PA), pro-urokinase (pro-UK), and urokinase (UK), and a twofold higher concentration of a plasmin-resistant mutant rpro-UK (Ala-158-pro-UK) was measured on a microtiter plate reader. The promoting effects on this reaction of equimolar concentrations of fibrinogen, soluble fibrin (Desafib), CNBr fragment FCB-2 (an analogue of fragment D), or purified fragment E-2 were compared. Plasmin generation by t-PA was moderately promoted by fibrinogen, substantially promoted by Desafib and FCB-2, but not at all promoted by fragment E-2. By contrast, plasmin generation by pro-UK or by Ala-158-pro-UK was not promoted either by fibrinogen, Desafib, or FCB-2, but was significantly promoted by fragment E-2. Plasmin generation by UK was not significantly promoted by any of the fibrin(ogen) preparations. Treatment of fragment E-2 by carboxypeptidase-B (CPB), eliminated its promotion of pro-UK and Ala-158-pro-UK-induced plasmin generation. Pretreatment of FCB-2 with plasmin slightly potentiated its promotion of t-PA activity. This effect of plasmin pretreatment of FCB-2 was reversed by CPB treatment. Plasmin pretreatment of FCB-2 did not induce any promotion of activity in pro-UK or Ala-158-pro-UK. The findings show that the intrinsic activity of pro-UK and the activity of t-PA are promoted by different regions of the fibrin(ogen) molecule. The latter is stimulated primarily by a determinant in the fragment D region, which is available in intact fibrin. By contrast, plasminogen activation by the intrinsic activity of pro-UK was stimulated exclusively by fragment E-2, which is unavailable in intact fibrin. The findings are believed relevant to fibrinolysis and support the concept that t-PA and pro-UK are complementary, sequential, and synergistic in their actions.

Carboxypeptidase B↗
PubMed1986

Tumor-initiating and promoting activities of di(2-ethylhexyl) phthalate in vivo and in vitro.

The carcinogenic effects of di(2-ethylhexyl) phthalate (DEHP), including its potential as an initiator and as a promoter of carcinogenesis, were studied in mouse liver and skin and in rat liver in vivo, and in mouse epidermis-derived JB6 cells in vitro. A mouse model for liver initiation and promotion involved initiation by injection of N-nitrosodiethylamine (DEN) intraperitoneally into male B6C3F1 mice at 4 weeks of age, followed by exposure to either DEHP in the diet (3000, 6000, or 12,000 ppm) or phenobarbital in the drinking water (500 ppm), beginning 1 to 2 weeks later and continuing for periods of from 1 day to 18 months. Female F344/NCr rats were subjected to a similar protocol in which promotion continued for 14 weeks. DEHP promoted focal hepatocellular proliferative lesions (FHPL), including hyperplastic foci and neoplasms initiated by DEN in mice but not in rats. Skin-painting studies in female CD-1 or SENCAR mice involved initiation by a single topical exposure to 7,12-dimethylbenz[a]-anthracene (DMBA) applied to the dorsal skin, followed by repeated percutaneous exposure to a tumor promoter, either DEHP or 12-O-tetradecanoylphorbol-13-acetate (TPA). To test for two-stage skin tumor promotion, SENCAR mice were initiated with DMBA and then TPA was administered for only 2 weeks, after which DEHP was subsequently administered for 26 weeks. DEHP displayed very weak complete promoting activity and definite second stage promoting activity in SENCAR mouse skin, but was inactive under our conditions on CD-1 mouse skin. In vitro promoting activity of DEHP and its hydrolysis products, mono(2-ethylhexyl) phthalate (MEHP) and 2-ethylhexanol (EH), was studied by using promotable mouse epidermis-derived JB6 cells. DEHP and MEHP promoted JB6 cells to anchorage independence, while EH did not.

Adenoma↗
PubMed1988

The role of promotion in alcoholism treatment marketing.

This article is an overview of the promotion function as a part of the ATM's marketing mix. It approaches various promotion decision areas from a managerial perspective, focusing upon some key components of promotion planning. Rather than provide specific operational or implementation details (how to write a brochure) it is more conceptual in nature and offers a framework for promotion planners. The article addresses promotion management, promotion objectives, analysis for promotion planning, the promotion mix, and addresses the benefits and limitations of some specific promotion tools available to the ATM manager. It treats ATMs as a service and reveals specific implications for promotion strategy dictated by services. The article also reports promotion tools employed by Alabama ATMs citing data from the Alabama study.

Advertising↗
PubMed1991

Cell transformation induced by bovine papillomavirus DNA as an assay for tumor promoters and chemopreventive agents.

An in vitro assay was designed to examine and quantitate the action of chemical promoters and chemopreventive agents on papillomavirus DNA-carrying cells. Cultured C3H/10T1/2 cells transfected with bovine papillomavirus type 1 DNA (plasmid pdBPV-1) were used as targets, and the frequency of transformed foci was used as an endpoint. The development of foci with a transformed phenotype was greatly enhanced by tumor promoters (e.g., mezerein, 12-O-tetradecanoyl-phorbol-13-acetate, teleocidin, and okadaic acid) and complex mixtures such as extracts of the areca nut, which is an integral part of a betel quid and is linked to oral cancers among chewers. The degree of promotion depended on the length of exposure, the type of promoter, and the time of application after transfection with BPV DNA. The inhibitory effect of chemopreventive agents on transformation can be tested either directly on BPV DNA transfected cells (promoter-independent transformation), or on transfected cells that were exposed to tumor promoters (promoter-dependent transformation). Retinol, and to a lesser degree beta-carotene, exerted an inhibitory effect on promoter-dependent and promoter-independent transformation of BPV DNA transfected cells. The inhibitory effect was conveyed either by the addition of retinol simultaneously with promoters, or after exposure to the promoting agents was completed. The significance of this short-term in vitro assay for the design of chemopreventive trials is discussed.

Animals↗
PubMed1985

Mechanism of mouse skin tumor promotion by chrysarobin.

The skin tumor-promoting ability of 1,8-dihydroxy-3-methyl-9-anthrone (chrysarobin) was compared with that of 12-O-tetradecanoylphorbol-13-acetate (TPA) and 1,8-dihydroxy-9-anthrone (anthralin) in SENCAR mice. Although dose-response comparisons indicated that chrysarobin was several orders of magnitude less potent than TPA for promoting papilloma formation, this anthrone was 1.5 to 2 times more potent than anthralin. Maximal papilloma responses were achieved by 15 weeks of promotion with TPA whereas at least 25 weeks of promotion were necessary to achieve maximal papilloma responses with chrysarobin or anthralin indicating marked differences in tumor latency between the two classes of compounds. Interestingly, at optimal promoting doses, chrysarobin gave a carcinoma response (22% with 0.3 carcinomas per mouse at 45 weeks) similar to that of TPA suggesting that this compound may be more efficient at promoting carcinomas than papillomas. In two-stage promotion experiments, chrysarobin was incapable of functioning independently as a Stage I or II promoter despite its complete promoting activity. Chrysarobin and TPA were compared at optimal promoting doses for their ability to induce: (a) skin edema, (b) epidermal hyperplasia, and (c) epidermal ornithine decarboxylase. In each case, distinct differences were noted between the two compounds. When taken together, the data support the hypothesis that anthracene-derived skin tumor promoters work at least in part by a mechanism different from the phorbol esters.

Animals↗
PubMed1980

Inhibition of induced differentiation of C3H/10T 1/2 clone 8 mouse embryo cells by tumor promoters.

C3H/10T 1/2 cells were induced to differentiate into muscle cells by treatment with 5-azacytidine, and the effects of tumor promoters, nonpromoters, and inhibitors of tumor promotion on this induced differentiation were investigated. Cell morphology was dramatically changed within 30 min after treatment with phorbol ester-related tumor promoters and mezereine but not with other tumor promoters. There was a good correlation between the tumor-promoting activity of the compounds and their inhibitory action on differentiation except in case of phenobarbital; this promoter of liver carcinogenesis did not inhibit differentiation. Inhibitors of tumor promotion, dexamethasone, fluocinolone acetonide, retinoic acid, and antipain, also inhibited the 5-azacytidine-induced differentiation. When the cells were treated after induction of differentiation with 12-O-tetradecanoylphorbol-13-acetate, a potent tumor promoter, and simultaneously with one of those inhibitors of tumor promotion, the inhibitory action of 12-O-tetradecanoylphorbol-13-acetate was not affected. From these facts, it is evident that using a single phenomenon produced by one class of tumor promoter as a criterion for screening environmental tumor promoters is not justifiable.

Animals↗
PubMedDate not supplied

[Dependence of the activity of phi X 174 B-promoter in the expression of Escherichia coli gal-operon on the number of its copies and their orientation].

Promoter activities of different restriction fragments of the R8 DNA region of phage phi X 174 were compared. The studied DNA fragments included HindII fragment R8 (B-promoter), its left portion 49 nucleotide long, and the central segment containing 113 nucleotides generated by AluI. The promoter activity of these fragments was quantitated by the appearance of uridyltransferase and galactokinase activities in Escherichia coli clones carrying plasmids pHD68-17. The gal-promoters of these plasmids was substituted for the three aforementioned restriction fragments. The R8 region and its central part (BII-promoter) had comparable promoter activities while the left part containing the putative BI-promoter, did not induce clones with the expressed gal-operon. Clones containing 1, 2, 3 copies of the promoter fragment R8 were selected. No clones were revealed with more copies. All selected di- and tri-promoter clusters in plasmids had the same correct orientation of all inserted promoters with respect to the gal-operon. The expression of the gal-operon in E. coli was nearly directly proportional to the number of the phi X 174 B-promoters inserted before the operon.

Bacteriophage phi X 174↗
PubMed1983

Molecular and cellular basis for tumor promotion in mouse skin.

Mouse skin painting studies have indicated that initiation-promotion protocols primarily yield benign tumors of monoclonal origin. The conversion of benign papillomas to carcinomas is not accelerated by promoters but is enhanced by mutagens. In contrast to initiation-promotion protocols, repeated application of complete carcinogens to mouse skin results in numerous carcinomas, and many of these cancers are multiclonal. These biological differences in tumor formation resulting from a promotion stage, as well as the reversibility of this stage, suggest an epigenetic mechanism of action for promoting agents. The monoclonal nature of the benign tumor indicates that cell selection may play an important role in tumor promotion. The ability to culture mouse epidermal cells has provided a model for delineating the mechanism of action of initiators and promoters. Exposure of cultured mouse keratinocytes to initiating agents results in cellular foci with altered behavior in which the cells resist the inhibitory growth signal associated with the induction of terminal differentiation. Such cells are also resistant to the induction of terminal differentiation in response to phorbol ester tumor promoters whereas subpopulations of normal keratinocytes are accelerated to differentiate by these agents. These differential responses to phorbol esters may be mediated by qualitative differences in phorbol ester receptors among keratinocyte subpopulations. Initiated cells appear to have unique phorbol ester receptor characteristics. Using oncogenic retroviruses as vectors, studies have been performed to assess the role of ras oncogene expression in initiation and promotion. An activated ras gene induces dramatic increases in epidermal basal cell proliferation, but such cells differ from initiated cells in that growth ceases in response to differentiation signals. While promoters can also enhance basal cell proliferation, they do not seem to induce a major increase in ras gene expression. We propose that the genetic change in the differentiation program induced by initiators provides a basis for selective clonal expansion of the initiated population by promoters to form a benign tumor. A subsequent genetic change, perhaps in the growth control program, may lead to malignant conversion. Altered expression of a ras gene may be relevant in this progression.

Animals↗
PubMed2000

PKC and ERK1/2 regulate amylase promoter activity during differentiation of a salivary gland cell line.

The addition of transforming growth factor alpha (TGFalpha) to a human submandibular gland cell line (HSG) cultured on basement membrane extract Matrigel, synergistically activates the acinar cell-specific salivary amylase promoter. Signaling through beta1 integrins and increased phosphorylation of ERK1/2 are involved in the increased promoter activity. Phorbol-12-myristate-13-acetate (PMA) and thapsigargin increase amylase promoter activity, suggesting that phorbol ester and calcium-dependent protein kinase C (PKC) pathways are also involved. The combination of specific inhibitors of PKC and MEK1 inhibits the amylase promoter. Inhibitors of the calcium-dependent PKC isoforms alpha, beta, and gamma decrease the promoter activity; however, PKCbeta is not detectable in HSG cells. TGFalpha alters the cellular localization of PKCalpha but not -gamma, suggesting PKCalpha is involved in TGFalpha upregulation of the amylase promoter. Furthermore, rottlerin, a PKCdelta-specific inhibitor, increases the promoter activity, suggesting PKC isoforms differentially regulate the amylase promoter. In conclusion, beta1-integrin and TGFalpha signaling pathways regulate the amylase promoter activity in HSG cells. In response to Matrigel and TGFalpha, the activation of both PKCalpha and phosphorylation of ERK1/2 results in synergistic activation of the amylase promoter. Published 2000 Wiley-Liss, Inc.

Amylases↗
PubMed1995

Structural and functional analysis of the promoter of the murine V gamma 1.1 T cell receptor gene.

The expression of the germ-line gene V gamma 1.1-C gamma 4 of the T cell receptor (TcR) gamma chain depends on interleukin (IL)-3 induction in hematopoietic cells, while in T cells, the rearranged gene is expressed constitutively. To understand the mechanism that controls TcR gamma gene expression, we cloned and characterized the structure and function of the V gamma 1.1-C gamma 4 TcR promoter. IL-3-dependent cell lines and T cell lines utilized the same transcriptional start sites. In chloramphenicol acetyltransferase (CAT) assays, the minimal 70-bp promoter confers strong transcriptional activity which is 50-60% of the Moloney long terminal repeat promoter activity. The 500-bp promoter region linked to the CAT gene exhibits IL-3 dependency similar to the endogenous TcR gamma gene. The immediate 3' and 5' flanking sequences inhibit the promoter activity two- to fourfold. The promoter lacks an obvious TATA box or CAAT box sequences, but contains a GC box in the untranslated region 3' to the promoter. The GC box is the core sequence of the element which binds Sp1-like proteins. Cloning of this Sp1 binding element in front of the thymidine kinase (TK) promoter and mutations generated in this site demonstrate its function as a silencer. Ultraviolet cross-linking analysis with the Sp1 binding site from the TcR gamma promoter revealed binding of a 90-100-kDa protein in a T cell line (EL-4) and 40-50 and 90-100-kDa proteins in FDC-P1 cells. The possible function of the Sp1-like protein in silencing the minimal promoter activity is discussed.

3T3 Cells↗
PubMed2006

Quantitative analysis of aromatase mRNA expression derived from various promoters (I.4, I.3, PII and I.7) and its association with expression of TNF-alpha, IL-6 and COX-2 mRNAs in human breast cancer.

The purpose of the present study was to study the aromatase mRNA expression as well as promoter usage (I.4, I.3, PII and I.7) in axillary adipose tissue (AA), mammary adipose tissue (MA), breast tumor tissue (BT) and adjacent normal breast tissue (NB), and to study the relationship between aromatase mRNA expression and tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and cyclooxygenase (COX)-2 mRNA expression. BT (n=108), NB (n=54), AA (n=41) and MA (n=34) from patients with breast cancer were subjected to real-time PCR assays for the mRNA levels of aromatase, TNF-alpha, IL-6 and COX-2. We also studied the usage of promoters I.4, I.3, PII and the recently reported endothelial promoter I.7. Total aromatase mRNA levels were significantly up-regulated in BT as compared with NB, AA and MA. Proportion of promoter l.4-specific transcripts against the total transcripts was significantly decreased and that of promoter l.3- and l.7-specific transcripts was significantly increased in BT than NB, AA and MA. However, the amount of transcripts from all the 4 promoters was significantly up-regulated in BT than NB, AA and MA. Estrogen receptor-alpha (ER-alpha) positive tumors showed a higher percentage of promoter I.7 usage than ER-alpha negative tumors with a marginal significance (p=0.05), and tumor with high microvessel counts tended (p=0.06) to show a higher percentage of promoter I.7 usage than those with low microvessel counts. There was a significant association between aromatase mRNA levels and TNF-alpha, IL-6 or COX-2 mRNA levels in BT, AA and MA but not in NB. These results suggest that enhanced transcription of promoters l.4, I.3, PII and I.7 explains the up-regulation of aromatase mRNA levels in BT. It has also been suggested that angiogenesis might stimulate the growth of ER-alpha positive tumors through the enhanced transcription of aromatase from promoter I.7 in endothelial cells in BT, and that TNF-alpha, IL-6 and COX-2 might be implicated in the up-regulation of aromatase mRNA in BT, AA and MA but not in NB.

Adipose Tissue↗
PubMed1985

Promotion of RNA transcription on the insertion element IS30 of E. coli K12.

Two promoters of RNA transcription have been identified on IS30 by an in vivo assay, in which various DNA fragments with IS30 sequences were inserted in front of the promoterless galK gene of plasmid pFD51. Both promoters have a similar activity of approximately 10% of the activity of the lacUV5 promoter. Promoter P30A precedes the long open reading frame (ORFA), and its proposed -35 region lies within the left-hand terminal inverted repeat of IS30. However, the apparent activity of promoter P30A is significantly reduced when measured in the 3' region of ORFA. Thus, either the activity of promoter P30A is controlled by an IS30-encoded product from the same element, or some termination of transcription from P30A occurs within the coding region of ORFA. Promoter P30C precedes a short open reading frame (ORFC) in-frame with ORFA, but in the opposite strand. Reading frame ORFC is closely followed by a terminator of RNA transcription, T30C. None of the other potential open reading frames predicted from the DNA sequence, with one possible exception, are preceded by a promoter of RNA transcription active in the assay. No significant transcription was detected out of the left-hand end of the complete element. However, a small amount, probably due to read-through from promoter P30A, was detected out of the right-hand end of a complete copy of IS30. In addition the right-hand end of IS30 has been shown to have the potential to create promoters by insertion.

Base Sequence↗
PubMed1990

Positive and negative functional interactions between promoter elements from different classes of RNA polymerase III-transcribed genes.

Consensus tRNA gene promoter elements, A and B boxes, were introduced into the coding sequence of a Xenopus U6 gene. Combinations in which A and B boxes were coupled to wild-type or mutant U6 promoters were made. In this way information about both the functions of individual promoter elements and functional relationships between different classes of RNA polymerase III promoter element were obtained. Mutants in which the U6 PSE was non-functional were rescued by the presence of a B box, indicating a degree of functional relationship between these two elements. Moreover, the B box acted to increase the transcriptional activity and competitive strength of the wild-type U6 promoter. In contrast, no evidence was obtained to suggest that a tRNA A box can interact productively with U6 promoter elements in the absence of a B box. Data obtained suggest that the U6 PSE functions as an 'adaptor', being necessary to enable the basal U6 promoter to respond to upstream enhancement. Certain combinations of U6 and tRNA promoter elements are shown to be mutually antagonistic by a mechanism which is likely to involve blockage of transcription initiation. In summary, the U6 and tRNA promoters are shown to consist of functionally related, but distinct, promoter elements whose interactions shed new light on their normal roles in transcription.

Animals↗