Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.6 (RNA polymerase)
34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When E. coli protein synthesis was blocked by chloramphenicol (100 micrograms/ml) or by essential amino acid deprivation, the transcription rates of rplKAJL genes (the ones for L11, L4, L10 and L7/L12 ribosomal proteins) and adjacent rpoBC genes (genes for RNA polymerase beta- and beta'-polypeptides) have been non-coordinately changed. The level of the gene transcription rate was obtained from RNA--DNA hybridization assays with E. coli pulse-labelled RNA and pJC703 or pJC720 plasmid DNA. The transcription of ribosomal protein genes has been found to be uncoupled with translation and controlled by the allelic state of relA gene. Conversely, the effective transcription of proBC gene was relA independent and coupled with translation of the mRNA. Chloramphenicol-induced transcription polarity within rplKAJL-rpoBC chromosome region can be suppressed by 10 micrograms/ml rifampicin.
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PMID:[Non-coordinated transcription of RNA polymerase beta,beta'-polypeptide genes and adjacent ribosomal protein genes in Escherichia coli cells]. 701 82

Sucrose density gradient centrifugation and DNA/RNA hybridization have been used to analyse the mRNA synthesized from the ribosomal protein - RNA polymerase subunits gene cluster rplKAJL-rpoBC in Escherichia coli. DNA/RNA hybrids obtained from total E. coli RNA and specific DNA restriction fragments from this chromosomal area were further subjected to endonuclease S1 digestion. This analysis permits the mapping of the ends of mRNA molecules for specific genes or operons by sizing the S1 resistant hybrids. Our results show that the predominant mRNA synthesized under conditions of balanced growth from the rplKAJL-rpoBC region codes for the four ribosomal proteins L11, L1, L10 and L7/12. This tetracistronic mRNA puts the transcription of the following rpoBC genes under the main control of the L11 promoter. Smaller distinct mRNA species could also be detected by this technique. They originate from intercistronic transcription termination and re-initiation as well as from processing of the larger polycistronic mRNA.
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PMID:In vivo synthesis of a polycistronic messenger RNA for the ribosomal proteins L11, L1, L10 and L7/12 in Escherichia coli. 703 27

A 6.5-kb DNA fragment containing the gene (rpoB) encoding the RNA polymerase (RNAP) beta subunit, from the mollicute Spiroplasma citri (Sc), was cloned and sequenced. The classical eubacterial organization, with the genes (rplK, A, J and L) encoding ribosomal proteins L11, L1, L10 and L12 located immediately upstream from rpoB, was not found in the Sc DNA. Instead, an open reading frame (hsdS) potentially encoding a component of a type I restriction and modification system was identified upstream from rpoB, and sequences showing similarities with insertion elements were found between hsdS and rpoB.
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PMID:The unique organization of the rpoB region of Spiroplasma citri: a restriction and modification system gene is adjacent to rpoB. 867 39

A 5018-bp DNA fragment of the rpl/rpo BC gene cluster (here called the rif cluster) of Streptomyces griseus N2-3-11 was analysed by DNA sequencing and transcription studies. By sequence comparison of the deduced proteins, five genes and part of an open reading frame (orf) were identified. The genes encoding the ribosomal (r-) proteins L1 (rplA), L7/12 (rplJ), L10 (rplK) and L11 (rplL), a protein of known function (orf31), and the N-terminus of the beta subunit of RNA polymerase (rpoB), are organized in three operons, rplKA, rplJL and rpoB(C), and the monocistronic transcription unit orf31. The promoters of these transcription units, rplKp, orf31p, rplJp, and rpoBp, were identified and the growth-phase dependence of the transcription of these operons was analysed. Binding sites for the ribosomal proteins L1 and L10 were identified by sequence comparison, suggesting that the r-proteins RplA and RplJ are involved in feedback regulation of their respective operons by binding to specific RNA-binding sites present in both the mRNA and the 23S rRNA, as has been described for other bacteria. The analyses of the rpoBp promoter by means of promoter-probe plasmids suggested a possible attenuator-based regulatory mechanism for the transcription of the rpoB(C) operon.
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PMID:Cloning and transcriptional analysis of the rplKA-or f31-rplJL gene cluster of Streptomyces griseus. 949 Oct 81

Growth-dependent regulation of rRNA synthesis is mediated by TIF-IA, a basal transcription initiation factor for RNA polymerase I. We inactivated the murine TIF-IA gene by homologous recombination in mice and embryonic fibroblasts (MEFs). TIF-IA-/- embryos die before or at embryonic day 9.5 (E9.5), displaying retardation of growth and development. In MEFs, Cre-mediated depletion of TIF-IA leads to disruption of nucleoli, cell cycle arrest, upregulation of p53, and induction of apoptosis. Elevated levels of p53 after TIF-IA depletion are due to increased binding of ribosomal proteins, such as L11, to MDM2 and decreased interaction of MDM2 with p53 and p19(ARF). RNAi-induced loss of p53 overcomes proliferation arrest and apoptosis in response to TIF-IA ablation. The striking correlation between perturbation of nucleolar function, elevated levels of p53, and induction of cell suicide supports the view that the nucleolus is a stress sensor that regulates p53 activity.
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PMID:Genetic inactivation of the transcription factor TIF-IA leads to nucleolar disruption, cell cycle arrest, and p53-mediated apoptosis. 1598 66

Guanosine tetraphosphate (ppGpp) is a key mediator of stringent control, an adaptive response of bacteria to amino acid starvation, and has thus been termed a bacterial alarmone. Previous X-ray crystallographic analysis has provided a structural basis for the transcriptional regulation of RNA polymerase activity by ppGpp in the thermophilic bacterium Thermus thermophilus. Here we investigated the physiological basis of the stringent response by comparing the changes in intracellular ppGpp levels and the rate of RNA synthesis in stringent (rel(+); wild type) and relaxed (relA and relC; mutant) strains of T. thermophilus. We found that in wild-type T. thermophilus, as in other bacteria, serine hydroxamate, an amino acid analogue that inhibits tRNA(Ser) aminoacylation, elicited a stringent response characterized in part by intracellular accumulation of ppGpp and that this response was completely blocked in a relA-null mutant and partially blocked in a relC mutant harboring a mutation in the ribosomal protein L11. Subsequent in vitro assays using ribosomes isolated from wild-type and relA and relC mutant strains confirmed that (p)ppGpp is synthesized by ribosomes and that mutation of RelA or L11 blocks that activity. This conclusion was further confirmed in vitro by demonstrating that thiostrepton or tetracycline inhibits (p)ppGpp synthesis. In an in vitro system, (p)ppGpp acted by inhibiting RNA polymerase-catalyzed 23S/5S rRNA gene transcription but at a concentration much higher than that of the observed intracellular ppGpp pool size. On the other hand, changes in the rRNA gene promoter activity tightly correlated with changes in the GTP but not ATP concentration. Also, (p)ppGpp exerted a potent inhibitory effect on IMP dehydrogenase activity. The present data thus complement the earlier structural analysis by providing physiological evidence that T. thermophilus does produce ppGpp in response to amino acid starvation in a ribosome-dependent (i.e., RelA-dependent) manner. However, it appears that in T. thermophilus, rRNA promoter activity is controlled directly by the GTP pool size, which is modulated by ppGpp via inhibition of IMP dehydrogenase activity. Thus, unlike the case of Escherichia coli, ppGpp may not inhibit T. thermophilus RNA polymerase activity directly in vivo, as recently proposed for Bacillus subtilis rRNA transcription (L. Krasny and R. L. Gourse, EMBO J. 23:4473-4483, 2004).
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PMID:Physiological analysis of the stringent response elicited in an extreme thermophilic bacterium, Thermus thermophilus. 1701 50

The c-Myc oncoprotein promotes cell growth by enhancing ribosomal biogenesis. Overexpression of c-Myc and aberrant ribosomal biogenesis lead to deregulated cell growth and tumorigenesis. Hence, c-Myc activity and ribosomal biogenesis must be tightly coordinated during normal homeostasis. We previously found that ribosomal protein L11 inhibits c-Myc activity by blocking the recruitment of its co-activator transformation/transcription domain-associated protein (TRRAP) to the promoter regions of c-Myc target genes that are transcribed by RNA polymerases I and II. In this study, we extended the role of L11 to the regulation of c-Myc-driven transcription of the 5 S rRNA and tRNA genes by RNA polymerase III. L11 co-resided with c-Myc at the 5 S rRNA and tRNA genes and significantly inhibited the binding of TRRAP to these genes. Knocking down endogenous L11 enhanced c-Myc-dependent transcription of these genes. Interestingly, in response to ribosomal stress induced by the treatment of cells with a low dose of actinomycin D or serum starvation, L11 binding to these genes was increased, and inversely TRRAP binding to these genes was decreased. Consistently, knockdown of L11 rescued the reduction of the expression of these genes by the two treatments. These results demonstrate that L11 suppresses c-Myc-dependent and RNA polymerase III-catalyzed transcription of 5 S rRNA and tRNA genes in response to ribosomal stress, ensuring a tight coordination between c-Myc activity and ribosomal biogenesis.
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PMID:Ribosomal protein L11 associates with c-Myc at 5 S rRNA and tRNA genes and regulates their expression. 2019 7

Ribosomal proteins (RPs) activate the p53 tumour-suppressor protein upon disruption of the nucleolus. However, the exact mechanisms for p53 transcriptional activation through RPs are not well understood. We show that the RPL11 is rapidly but transiently recruited at promoter sites of p53-regulated genes upon nucleolar stress induced by actinomycin D (ActD). Characterisation of molecular events at p53 promoter sites shows that L11 is required for the recruitment of p53 transcriptional co-activators p300/CBP and p53 K382 acetylation. We found that direct binding to Mdm2 E3 ligase and NEDDylation of L11 are critical regulators for L11 promoter recruitment. Our data suggest that binding of L11 to Mdm2 at the promoter results in relief from Mdm2-mediated transcriptional repression of p53. Analysis of chromatin and RNA polymerase II markers suggests that L11 is involved in the initiation step of transcriptional activation. Furthermore, analysis of 36 ActD-induced genes shows that L11 and NEDD8 are global regulators of the p53 activation response. The studies provide insights on how nucleolar stress through L11 and NEDD8 can activate the transcriptional activity of p53.
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PMID:Recruitment of RPL11 at promoter sites of p53-regulated genes upon nucleolar stress through NEDD8 and in an Mdm2-dependent manner. 2208 Oct 73

Cell cycle regulation is a very accurate process that ensures cell viability and the genomic integrity of daughter cells. A fundamental part of this regulation consists in the arrest of the cycle at particular points to ensure the completion of a previous event, to repair cellular damage, or to avoid progression in potentially risky situations. In this work, we demonstrate that a reduction in nucleotide levels or the depletion of RNA polymerase I or III subunits generates a cell cycle delay at the G1/S transition in Saccharomyces cerevisiae. This delay is concomitant with an imbalance between ribosomal RNAs and proteins which, among others, provokes an accumulation of free ribosomal protein L5. Consistently with a direct impact of free L5 on the G1/S transition, rrs1 mutants, which weaken the assembly of L5 and L11 on pre-60S ribosomal particles, enhance both the G1/S delay and the accumulation of free ribosomal protein L5. We propose the existence of a surveillance mechanism that couples the balanced production of yeast ribosomal components and cell cycle progression through the accumulation of free ribosomal proteins. This regulatory pathway resembles the p53-dependent nucleolar-stress checkpoint response described in human cells, which indicates that this is a general control strategy extended throughout eukaryotes.
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PMID:Balanced production of ribosome components is required for proper G1/S transition in Saccharomyces cerevisiae. 2404 28


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