Transcriptional Regulation of Genes Organized in the CytR Regulon of Escherichia Coli PDF Download
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Author: Hans-Henrik Kristensen
Publisher:
ISBN:
Category :
Languages : en
Pages :
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Author: Hans-Henrik Kristensen
Publisher:
ISBN:
Category :
Languages : en
Pages :
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Author: E. C. C. Lin
Publisher: Springer Science & Business Media
ISBN: 1468486012
Category : Medical
Languages : en
Pages : 1010
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This up-to-date guide focuses on the understanding of key regulatory mechanisms governing gene expression in Escherichia coli. Studies of E. coli not only provide the first models of gene regulation, but research continues to yield different control mechanisms.
Author: Allison Kathryn Holt
Publisher:
ISBN: 9780549981053
Category :
Languages : en
Pages : 344
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This approach allowed us to correlate reported levels of activation, repression and induction with the ligation states of these five promoters under physiologically relevant conditions. A general pattern of transcriptional regulation emerges that allows for complex patterns of regulation in this seemingly simple system.
Author: Weiyin Shen
Publisher:
ISBN:
Category : Escherichia coli
Languages : en
Pages : 334
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Author: Thomas Edward Kuhlman
Publisher:
ISBN: 9781109953855
Category :
Languages : en
Pages : 200
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In Chapter 4, Quantitative Characteristics of Gene Regulation by Small RNA, we study quantitatively two classes of bacterial small RNAs (sRNA) in Escherichia coli. We demonstrate that sRNA provide a novel mode of gene regulation with characteristics distinct from those of protein-mediated gene regulation. These include a threshold-linear response with a tuneable threshold and a built-in capability for hierarchical cross talk.
![Transcriptional Regulation and Autogenous Control of the Genes for the ß and ß' Subunits of Escherichia Coli RNA Polymerase [microform] PDF](https://books.google.com/books/content/images/frontcover/ONjgwQEACAAJ?fife=w80-h100)
Author: Steward, Keith L., 1962
Publisher: National Library of Canada = Bibliothèque nationale du Canada
ISBN: 9780315905924
Category :
Languages : en
Pages : 230
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The transcriptional control of the two genes rpoB and rpoC encoding the $\beta$ and $\beta\sp\prime$ subunits of RNA polymerase was examined in a systematic fashion in order to evaluate the contribution of such control to the autogenous regulation of RNA polymerase synthesis. Numerous transcriptional fusions were constructed by placing restriction fragments of the rplKaJLrpoBC gene cluster upstream of the lacZ reporter gene on $\lambda$ phage vectors. Assaying $\beta$-galactosidase activity from monolysogens of the recombinant phage permitted a high resolution scan of the gene cluster for transcriptional controls. The results precisely quantitate the efficiencies of two strong promoters, rplKp and rplJp, a weak promoter rplLp, and a transcriptional attenuator rpoBa located between rplL and rpoB. From this data, the relative contribution of each transcriptional signal to the overall transcription of rpoBC was determined. It was found that almost all transcription initiated from the strong rplKp promoter continued into the downstream rplJLrpoB genes; that rplJp continues to initiate efficiently despite such transcription from the upstream promoter; and most surprisingly, that the efficiency of termination at the rpoBa attenuator depended on whether transcription was initiated from rplKp, rplJp, or both promoters. Further examination of the latter phenomenon revealed that the efficiency of rpoBa was related in an inverse fashion to the frequency of transcription initiated by promoters located upstream of it. When the frequency of transcription into the attenuator was decreased over a 40-fold range by replacing rplJp and rplKp with alternative promoters, readthrough at rpoBa increased from 19% to 61%. When regions located upstream of rpoBa are deleted or inverted, the modulation of rpoBa may be abrogated. In addition, sequence analysis of the region can identify a site with remarkable homology to the boxB motif of the $\lambda\ nutR$ site. Such findings suggest the potential involvement of antitermination in the modulation of rpoBa function. Modulation of rpoBa, together with the evidence by others that the global frequency of transcription is influenced by the cellular concentration of RNA polymerase, suggests that rpoBa may play a role in the autogenous control of rpoBC expression.
Author: Lok-hang So
Publisher:
ISBN:
Category :
Languages : en
Pages :
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The blueprint of a living cell is inscribed in its DNA. A region of DNA encoding a protein is called a gene. The cell reads the DNA and makes molecular machines made up of proteins to carry out all cellular functions required for survival. All cells live in ever-changing environments, and have different needs at different times. The control of when and how often each protein is produced from a gene is called gene regulation. Transcription, the copying of a DNA sequence into a complementary mRNA molecule, is the first step in the information flow from DNA to proteins, and most regulation is already done at the transcription level to avoid the production of superfluous intermediates. A living cell takes environmental stimuli as input, and regulates the activity of genes through DNA-binding proteins called transcription factors. The activity of a gene is described by its time-series of discrete mRNA production events. The events constituting this transcriptional time-series are stochastic and exhibit intermittent, bursty behavior, in bacteria as well as higher organisms. Thus the transcriptional time-series cannot be fully described by a simple chemical 0́−rate0́+0́4the probability per unit time of transcribing an mRNA molecule. An important consequence of this temporal complexity is that gene expression level can be tuned by varying different features of the time-series. It is then natural to ask: What modulation scheme is used by the cell to change expression levels of genes? Furthermore, if we look at the transcriptional time-series of multiple genes, would we see different modulation schemes for different genes, or a common modulation scheme shared by all genes? Last but not least, what is the molecular mechanism leading to bursty transcriptional time-series? What are the biophysical states that correspond to the active and inactive periods in a bursty transcriptional time-series? To answer these questions, I characterized the mRNA copy-number statistics from multiple promoters in the model organism Escherichia coli under various growth conditions using single-molecule fluorescence in situ hybridization. The kinetics of the underlying transcriptional time-series was then inferred using the two-state model, a simple stochastic mathematical model that describes bursty transcription time-series. I found that the degree of burstiness depends only on the gene expression level, while being independent of the details of gene regulation. The observed behavior is explained by the underlying variation in the duration of bursting events. At this stage, there is no mechanistic, molecular-level understanding of what gives rise to the bursty behavior of gene activity in bacteria. However, my finding here, that the properties of the transcriptional time-series are gene-independent rather than gene-specific, is contrary to the most common theoretical model used to explain bursty transcriptional time-series in bacteria, which involves the binding and unbinding of transcription factors at the promoter. My data suggests that the observed bursty kinetics arises from gene-nonspecific mechanisms such as DNA topology modulation, RNA polymerase dynamics, or regulation by broad-target DNA-binding proteins. Further investigation would narrow down the source of bursty transcriptional time-series.
Author: Susanne Horsevad Jensen
Publisher:
ISBN:
Category :
Languages : en
Pages : 110
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Author: Hemali Bharat Patel
Publisher:
ISBN:
Category :
Languages : en
Pages : 392
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Abstract: The stringent response is a response network in bacteria that is triggered by nutrient limitation and involves a global reprogramming of gene transcription, orchestrated largely by a signaling molecule guanosine tetraphosphate (ppGpp). Despite decades of studies on individual genes perturbed during the stringent response in Escherichia coli, the characteristic transcriptional profile and the role of ppGpp in affecting global transcriptional changes during the stringent response had remained to be determined systematically. We provoked the stringent response, in the strain E. coli K-12, by multiple induction pathways and identified the core transcriptional profile that is characteristic of the cellular response to ppGpp accumulation. By comparison of wild type and ppGpp-deficient E. coli mutant strains, we identified the gene expression changes that are specifically dependent upon ppGpp. We found six transcriptional regulators that are recruited in the core stringent response. We show the regulatory targets of one of these six regulators, RpoS. Over 80% of transcriptional regulation was directly or indirectly dependent upon the general stress response sigma factor, RpoS, even in presence of ppGpp. Our findings suggest that ppGpp alone is not capable of mounting a global stringent response, and it relies heavily on transcriptional regulators such as RpoS. Existing regulatory models for ppGpp-mediated regulation suggest a global redistribution of RNA polymerase (RNAP), upon binding with ppGpp, during stringent response. We have shown evidence for such redistribution of RNAP in presence of ppGpp by conducting ChIP-chip analysis of ppGpp-rich and ppGpp-deficient cells with an antibody specific to the alpha-subunit of RNAP. We also correlated transcriptional changes with a phenotype of increased viability in acidic medium, and demonstrated that it was dependent upon both ppGpp and RpoS. We have shown that ppGpp enhances long-term survival, up to two hours, in acid. Our results reveal the significance of stringent response in development of phenotypes that facilitate adaptation in acidic host environments for E. coli.
Author:
Publisher:
ISBN:
Category : Medicine
Languages : en
Pages : 1100
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