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In vitro assay for tumor promoters and anti-promoters.

Tumor promoters and anti-promoters have been shown to modify the induction of ornithine decarboxylase, the production of plasminogen activator, and the recovery of induced mutations. Data were presented to show that the recovery of mutagen-induced ouabain-resistant mutations in cultured Chinese hamster cells is increased with a tumor-promoter treatment and reduced by anti-promoter treatments. The results suggest that many induced mutations can either be repressed or derepressed by promoters or anti-promoters. The results also support the hypothesis that tumor initiation is due to a mutagenic event, while tumor promotion is the result of an epigenetic process involving cyclic nucleotide modulation of gene expression.

Animals↗
PubMed1976

Effect of stringent and relaxed control on transcription of the tryptophan operon from the ptrp promoter and the PL promoter in trp phage.

Tryptophan (trp) mRNA synthesis from the authentic trp promoter (Ptrp) is apparently arrested upon translation blockage, while trp mRNA synthesis as a result of read-through from the Pl promoter of the N gene in trp phage is not so affected. When translation is blocked at a nonpermissive temperature in the temperature-sensitive mutants of Escherichia coli rel carrying altered ribosomal elongation factors G (strain CP78G) and Ts (strain HAK88), CP78G and HAK88 show relaxed and stringent phenotypes respectively in control of RNA synthesis. Under conditions causing translation blockage in both mutants, Pl-promoted synthesis of trp mRNA is not depressed while Ptrp-promoted synthesis of trp mRNA is blocked. The insensitivity of Pl-promoted transcription of the translocated trp operon to stringent control is also confirmed by using a strain 10b6s rel carrying a temperature-sensitive valyl-tRNA synthetase. In contrast to the above observation, transcription of the trp operon from either the Pl and Ptrp promoters in a 10b6r rel infected with trp is inhibited greatly at the nonpermissive temperature. This effect occurs even if the level of trp transcription observed at 30 degrees is already low, thus suggesting that translational machinery is intrinsically abnormal in the rel strain.

Coliphages↗
PubMed1979

Construction and characterization of E. coli promoter-probe plasmid vectors. I. Cloning of promoter-containing DNA fragments.

Derivatives of the Escherichia coli drug-resistance plasmid pBR316 have been constructed which act as molecular probes for promoter-containing DNA restriction fragments from various prokaryotic genomes. The plasmids, designated pBRH1 and pBRH3B, contain a unique EcoRI restriction site located within the promoter for the tetracycline resistance (Tcr) gene. This site was created by the insertion of a chemically synthesized octanucleotide, containing the EcoRI cleavage sequence, into the HindIII site of pBR316. Base-pair alterations within the Tc promoter produced by this insertion resulted in a substantial reduction (pBRH3B) or elimination (pBRH1) in ability of these plasmids to confer Tc resistance to the host strain. Cloning of EcoRI-cleaved foreign DNA fragments into the EcoRI site of these plasmids allows for the isolation of recombinant transformants with Tcr levels greater than that of the plasmid vector. Further characterization of these recombinant plasmids demonstrates that the Tcr phenotype is dependent upon the orientation of the inserted fragment, but not on the molecular weight. We have concluded that these fragments carry promoters which, in the proper orientation, allow for the transcription of the Tcr gene. The utility of these "promoter-probe" plasmids lies in the ability to select for promoter-containing DNA fragments by insertional activation of the Tcr gene.

Bacillus subtilis↗
PubMed1977

Dissociation of tumor promoter-stimulated ornithine decarboxylase activity and DNA synthesis in mouse epidermis in vivo and in vitro by fluocinolone acetonide, a tumor-promotion inhibitor.

12-O-Tetradecanoyl phorbol-13-acetate (TPA), a tumor promoter, stimulates DNA synthesis in mouse epidermal cells in vivo and in vitro. This response appears to be mediated through polyamine metabolism because ornithine decarboxylase (L-ornithine carboxy-lyase, EC 4.1.1.17)activity is markedly increased shortly after promoter exposure and this induction varies in magnitude according to dose and promoter potency of a series of phorbol esters. In vitro, exogenous putrescine (0.01-10 mM) results in a dose-related increase and prolongation of promoter-stimulated DNA DNA synthesis, a phenomenon noted in other systems of polyamine-mediated growth stimulation. The anti-inflammatory steroid fluocinolone acetonide (FA), an inhibitor of tumor promotion, prevents TPA stimulation of epidermal proliferation in vivo and in vitro. In vitro, FA most effectively prevents stimulation of DNA synthesis when applied is not required. Paradoxially, FA potentiates the increase in ornithine decarboxylase activity after TPA administeration both in vivo and in vitro. Furthermore, the inhibition of TPA-stimulated DNA synthesis by FA in vitro can be reversed by exogenous putrescine. These results suggestthat FA exerts its antipromotion effect by reducing the sensitivity of the cell to polyamines or by reducing intracellular polyamine levels.

Animals↗
PubMed1977

The araC promoter: transcription, mapping and interaction with the araBAD promoter.

The start sites of the araC and araBAD gene messenger of E. coli were located by transcription in vitro from short DNA fragments, by high magnification electron microscopy and by genetic mapping. Transcription for these messengers proceeds in opposite directions from the start sites that are 150 base pairs apart. Transcription from the araBAD promoter requires araC protein plus arabinose and CAP protein plus cyclic AMP. In the experiments performed in vitro, inducing the araBAD promoter represses activity of the araC promoter.

Arabinose↗
PubMed2026

Nucleolin promotes neuropathic pain by increasing chromatin accessibility at the Ccl2 promoter in primary sensory neurons.

Nerve injury-induced transcriptional alterations in primary sensory neurons of the dorsal root ganglion (DRG) constitute a key molecular basis for the development of neuropathic pain. Nucleolin (NCL), a highly conserved multifunctional nucleolar protein, regulates gene transcription. Here, we identify that NCL is expressed exclusively in the nuclei of DRG neurons. Peripheral nerve injury time-dependently upregulates Ncl mRNA and NCL protein levels in injured DRG neurons. Blocking this upregulation through DRG microinjection of the adeno-associated virus 9 (AAV9) expressing an shRNA targeting Ncl attenuates nerve injury-induced increases of C-C motif chemokine ligand 2 (CCL2) mRNA and its protein in injured DRG and alleviates the development and maintenance of mechanical, heat and cold hypersensitivities. Conversely, mimicking DRG NCL upregulation through DRG microinjection of AAV9 carrying the full-length Ncl coding sequence increases Ccl2 mRNA and CCL2 protein levels in microinjected DRGs and produces neuropathic pain-like symptoms in the absence of nerve injury. Mechanistically, peripheral nerve injury increases NCL occupancy at the Ccl2 promoter and enhances chromatin accessibility at this locus, resulting in elevated CCL2 expression in injured DRG neurons, which is reversed by NCL knockdown. Given that Ncl mRNA is co-expressed with Ccl2 mRNA in individual DRG neurons, our findings suggest that NCL upregulation in the DRG contributes to neuropathic pain likely by increasing chromatin accessibility at the Ccl2 promoter in primary sensory neurons.

Animals↗
PubMed1979

Bacteriophage lambda-E. coli K12 vector-host system for gene cloning and expression under lactose promoter control. II. DNA fragment insertion at the vicinity of the lac UV5 promoter.

Bacteriophage vectors derived from lambda plac5 have been constructed. Their genomes have one EcoRI restriction site which is located at the very beginning of the lac Z gene. The major part of this gene was deleted by an in vivo intramolecular recombination. These vectors allow the fusion of a gene or an operon with the beginning of the lac Z gene, placing them under the control of the lac promoter, which carries the UV5 mutation. Some of these vectors (lambda Y) also include the lac Y gene and it too is under the control of the lac promoter. The lambda YEQS, which carries the Qam73 and Sam7 mutations, as safety mutations, has been certified as a B2 (EK2) vector by the French control commission "recombinaison génétique in vitro".

Coliphages↗
PubMed1979

Construction of plasmid cloning vehicles that promote gene expression from the bacteriophage lambda pL promoter.

Two multiple-copy, ColE1-type, plasmid cloning vehicles, pHUB2 and pHUB4, have been constructed that carry four different single restriction sites down-stream from the phage lambda promoter pL. The promoting activity of pL is switched off at low temperature in the presence of a cIts gene that specifies a temperature-sensitive repressor but could be activated by heat induction. cIts was located either on the host chromosome, or on a second plasmid pRK248 that is compatible with the cloning vehicle, or on the vehicle itself. Three different restriction fragments, each carrying the gene trpA of Salmonella typhimurium or Shigella dysenteriae, have been inserted into the EcoRI, BamHI and SalI sites, respectively, of these plasmids and pL dependent expression of the inserted gene in Escherichia coli was determined by measuring the enzymatic activity of the trpA gene product. Heat induction resulted in a level of expression of trpA corresponding to 1 to 6.6% of the total soluble cell protein as trpA protein. The level of trpA protein production depended on the particular insert and the plasmid used.

Bacterial Proteins↗
PubMed1979

In vivo transcription of rRNA operons in Escherichia coli initiates with purine nucleoside triphosphates at the first promoter and with CTP at the second promoter.

32P-labeled RNA was isolated from growing Escherichia coli and the 5' end nucleoside triphosphates of rRNA were analyzed after hybridization to various DNA fragments derived from one of the rRNA operons, rrnE. The results show that there are two transcription start sites for each rRNA operon in vivo, one initiating with ATP (or GTP), and the second initiating with CTP. Transcription from the first site was observed to be stronger than that from the second site. These two sites correspond to the two promoters identified in the previous in vitro studies, indicating that the two promoters are used in vivo. These results also demonstrate previously unrecognized transcription initiation with CTP in growing E. coli cells.

Cytidine Triphosphate↗
PubMed1977

Enhancement of the DNA synthetic response of antigen-primed lymph node cells by splenic promoter cells: characterization of the splenic promoter cells.

Rabbits were immunized in the footpad with diphtheria toxoid in complete Freund's adjuvant. At various times after immunization, cells harvested from the spleen, the draining (immune) and the opposing (control) lymph nodes (LN) were assayed for their proliferative response to incorporate tritiated thymidine upon exposure to the priming antigen. Although the immune LN cells responded by a substantial incorporation of thymidine, cells from the control LN and the spleen either did not respond or responded feebly. An enhancement in the response of the immune LN cells was observed when they were cultured in the presence of nonresponsive spleen cells. Pretreatment of spleen cells with mitomycin C did not abolish the enhancement. This suggests that the target cells which respond to the antigen are derived from the immune LN whereas the promoter cells which enhance the response are present in the spleen. The removal of adhering cells by glass wool columns and of Ig-bearing cells by anti-Ig immunoabsorbent columns from the spleen did not reduce the enhancing capacity of the nonadhering cells. Conversely, the killing of splenic T cells by specific heterologous antiserum directed against rabbit thymus lymphocyte antigen abolished the enhancement. Thus, the promoter cell which facilitates the enhancement has been characterized as a nonadherent, splenic T cell.

Animals↗
PubMed2025

Hepatocyte-Enriched miRNA-193b-3p Promotes Hepatitis B Virus Replication by Dual Activation of Viral Core Promoter Activity and Autophagy Induction by Targeting IGF-1R.

Hepatitis B virus (HBV) infection is a principal cause of severe liver disease in humans and is associated with increased levels of specific serum or intracellular microRNAs (miRNAs). Among these, miR-193b-3p is a liver-enriched miRNA; however, its role in HBV replication remains unknown. This study aimed to investigate the influence of chronic HBV infection on miR-193b-3p levels in the peripheral blood and liver tissues of patients with chronic hepatitis B (CHB), evaluate the effect of miR-193b-3p on HBV replication both in vitro and in vivo, and elucidate the potential underlying mechanisms. We showed that hepatic miR-193b-3p levels in patients with CHB were significantly elevated compared with those in healthy controls. Ectopic expression of miR-193b-3p significantly enhanced HBV replication and transcription in different hepatoma cell lines. Furthermore, we identified IGF-1R as a direct target through which miR-193b-3p regulates HBV replication. Mechanistically, miR-193b-3p increased HBV core promoter activity via the IGF-1R/FXRα axis, thereby enhancing HBV transcription. Additionally, miR-193b-3p increased IGF-1R/Akt/MDM2/p53 signaling-mediated autophagy induction, which in turn facilitated increased HBV post-transcriptional activity. Collectively, hepatocyte-enriched miR-193b-3p exerts a proviral effect on HBV replication through dual synergistic mechanisms, offering novel insights into its role in HBV replication and potential therapeutic implications in CHB infection.

Humans↗
PubMed1979

Gastric carcinoma promoted by alkaline reflux gastritis -- with special reference to bile and other surfactants as promoters of postoperative gastric cancer.

For reasons that are not known, the incidence of stomach cancer is declining in most countries. In contrast, cancer of the gastric remnant after partial gastrectomy for peptic ulcer disease seems to be increasing. "Stump cancer" has been claimed to be a separate disease entity and has recently been mentioned as an iatrogenic cancer. Alkaline bile reflux, dietary surfactants and maybe the abuse of tobacco are postulated as promoting or initiating agents, in causing malignant transformation of the operated as well as non-operated stomach. Variations in gastric pH, microflora and emptying rate may be of importance in the carcinogenic process. The decline in cancer incidence in the non-operated stomach has mainly been restricted to the intestinal type of cancer. Thus, it is important to note that stump cancer often is of the diffuse type. Different target cells and/or modes of carcinogen exposure may be of etiological importance in these histologically and clinically separate neoplastic diseases.

Animals↗
PubMed1978

Attempts at analysis of toxicity of pertussis vaccine. III. Effects of endotoxin on leukocytosis in mice due to lymphocytosis-promoting factor and reference preparations for determination of lymphocytosis-promoting factor.

The effect of bacterial endotoxin on the change in peripheral leukocyte population in mice due to the lymphocytosis-promoting factor (LPF) was investigated. Endotoxin affected not only the total leukocyte count but also the leukocyte proportions at any observation time. Both the coefficient and the intercept of regression of the leukocytic response on dose of LPF were modified by endotoxin. Therefore, in a valid biological assay for LPF using the peripheral leukocyte count as a response, a common reference preparation available for any test materials, irrespective of presence or absence of endotoxin, will be impracticable. Two reference preparations were tentatively established, one being a vaccine and the other an LPF preparation containing little endotoxin. A unitage of LP activity was assigned to each reference preparation. The results also showed that an LPF material to be tested for its possible effects on the lymphatic tissues or the reticuloendothelial system should be free from endotoxin.

Animals↗
PubMed1978

PL-promoted transcription of the promoter-proximal N-trp region is insensitive to chloramphenicol in the absence of N function.

When the trp operon is translocated into the early region of lambda phage, transcription originated at the PL promotor is known to be modified by function of the N gene product so that transcription of the operon continues when translation is blocked by nonsense mutations or by ribosomal antibiotics. When N function is deficient in a phage that joins the trp operon to a point distal to the N gene, deleting the tL site, nonsense mutations (Franklin, 1974) or chloramphenicol (Nakamura et al., accompanying paper) again block transcription of the bacterial operon. However, here we report that transcription over about the first 800 nucleotide pairs starting from the PL promotor of the N-trp operon is still insensitive to chloramphenicol even in the absence of N function. The region covers the full N gene and the initial bit of the trp operon.

Chloramphenicol↗