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  • 1
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    Selective transcriptional regulation by Myc in cellular growth control and lymphomagenesis (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-07-22
    Description: The c-myc proto-oncogene product, Myc, is a transcription factor that binds thousands of genomic loci. Recent work suggested that rather than up- and downregulating selected groups of genes, Myc targets all active promoters and enhancers in the genome (a phenomenon termed 'invasion') and acts as a general amplifier of transcription. However, the available data did not readily discriminate between direct and indirect effects of Myc on RNA biogenesis. We addressed this issue with genome-wide chromatin immunoprecipitation and RNA expression profiles during B-cell lymphomagenesis in mice, in cultured B cells and fibroblasts. Consistent with long-standing observations, we detected general increases in total RNA or messenger RNA copies per cell (hereby termed 'amplification') when comparing actively proliferating cells with control quiescent cells: this was true whether cells were stimulated by mitogens (requiring endogenous Myc for a proliferative response) or by deregulated, oncogenic Myc activity. RNA amplification and promoter/enhancer invasion by Myc were separable phenomena that could occur without one another. Moreover, whether or not associated with RNA amplification, Myc drove the differential expression of distinct subsets of target genes. Hence, although having the potential to interact with all active or poised regulatory elements in the genome, Myc does not directly act as a global transcriptional amplifier. Instead, our results indicate that Myc activates and represses transcription of discrete gene sets, leading to changes in cellular state that can in turn feed back on global RNA production and turnover.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110711/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110711/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabo, Arianna -- Kress, Theresia R -- Pelizzola, Mattia -- de Pretis, Stefano -- Gorski, Marcin M -- Tesi, Alessandra -- Morelli, Marco J -- Bora, Pranami -- Doni, Mirko -- Verrecchia, Alessandro -- Tonelli, Claudia -- Faga, Giovanni -- Bianchi, Valerio -- Ronchi, Alberto -- Low, Diana -- Muller, Heiko -- Guccione, Ernesto -- Campaner, Stefano -- Amati, Bruno -- 10-0245/Worldwide Cancer Research/United Kingdom -- 268671/European Research Council/International -- England -- Nature. 2014 Jul 24;511(7510):488-92. doi: 10.1038/nature13537. Epub 2014 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Via Adamello 16, 20139 Milan, Italy [2] Department of Experimental Oncology, European Institute of Oncology (IEO), Via Adamello 16, 20139 Milan, Italy [3]. ; 1] Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Via Adamello 16, 20139 Milan, Italy [2]. ; Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Via Adamello 16, 20139 Milan, Italy. ; Department of Experimental Oncology, European Institute of Oncology (IEO), Via Adamello 16, 20139 Milan, Italy. ; Institute of Molecular and Cell Biology, Singapore 138673, Singapore. ; 1] Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Via Adamello 16, 20139 Milan, Italy [2] Department of Experimental Oncology, European Institute of Oncology (IEO), Via Adamello 16, 20139 Milan, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043028" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism/pathology ; *Cell Proliferation ; Cell Transformation, Neoplastic/*genetics/pathology ; Chromatin/genetics/metabolism ; Chromatin Immunoprecipitation ; Disease Progression ; Down-Regulation/genetics ; Female ; Fibroblasts/cytology/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Neoplastic/genetics ; Genome/genetics ; Lymphoma, B-Cell/*genetics/metabolism/*pathology ; Male ; Mice ; Mitogens/pharmacology ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins c-myc/genetics/*metabolism ; RNA, Messenger/biosynthesis/genetics/metabolism ; Transcription Factors/metabolism ; *Transcription, Genetic/genetics ; Up-Regulation/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Using combined evidence from replicates to evaluate ChIP-seq peaks (2015)
    Oxford University Press
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    Publication Date: 2015-08-25
    Description: Motivation: Chromatin Immunoprecipitation followed by sequencing (ChIP-seq) detects genome-wide DNA–protein interactions and chromatin modifications, returning enriched regions (ERs), usually associated with a significance score. Moderately significant interactions can correspond to true, weak interactions, or to false positives; replicates of a ChIP-seq experiment can provide co-localised evidence to decide between the two cases. We designed a general methodological framework to rigorously combine the evidence of ERs in ChIP-seq replicates, with the option to set a significance threshold on the repeated evidence and a minimum number of samples bearing this evidence. Results : We applied our method to Myc transcription factor ChIP-seq datasets in K562 cells available in the ENCODE project. Using replicates, we could extend up to 3 times the ER number with respect to single-sample analysis with equivalent significance threshold. We validated the ‘rescued’ ERs by checking for the overlap with open chromatin regions and for the enrichment of the motif that Myc binds with strongest affinity; we compared our results with alternative methods (IDR and jMOSAiCS), obtaining more validated peaks than the former and less peaks than latter, but with a better validation. Availability and implementation : An implementation of the proposed method and its source code under GPLv3 license are freely available at http://www.bioinformatics.deib.polimi.it/MSPC/ and http://mspc.codeplex.com/ , respectively. Contact : marco.morelli@iit.it Supplementary information: Supplementary Material are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 3
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    INSPEcT: a computational tool to infer mRNA synthesis, processing and degradation dynamics from RNA- and 4sU-seq time course experiments (2015)
    Oxford University Press
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    Publication Date: 2015-08-25
    Description: Motivation: Cellular mRNA levels originate from the combined action of multiple regulatory processes, which can be recapitulated by the rates of pre-mRNA synthesis, pre-mRNA processing and mRNA degradation. Recent experimental and computational advances set the basis to study these intertwined levels of regulation. Nevertheless, software for the comprehensive quantification of RNA dynamics is still lacking. Results: INSPEcT is an R package for the integrative analysis of RNA- and 4sU-seq data to study the dynamics of transcriptional regulation. INSPEcT provides gene-level quantification of these rates, and a modeling framework to identify which of these regulatory processes are most likely to explain the observed mRNA and pre-mRNA concentrations. Software performance is tested on a synthetic dataset, instrumental to guide the choice of the modeling parameters and the experimental design. Availability and implementation: INSPEcT is submitted to Bioconductor and is currently available as Supplementary Additional File S1 . Contact: mattia.pelizzola@iit.it Supplementary Information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 4
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    DNA looping provides stability and robustness to the bacteriophage   switch (2009)
    National Academy of Sciences
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    Publication Date: 2009-05-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    Ultradeep Sequencing Analysis of Population Dynamics of Virus Escape Mutants in RNAi-Mediated Resistant Plants (2012)
    Oxford University Press
    Details
    Publication Date: 2012-10-17
    Description: Plant artificial micro-RNAs (amiRs) have been engineered to target viral genomes and induce their degradation. However, the exceptional evolutionary plasticity of RNA viruses threatens the durability of the resistance conferred by these amiRs. It has recently been shown that viral populations not experiencing strong selective pressure from an antiviral amiR may already contain enough genetic variability in the target sequence to escape plant resistance in an almost deterministic manner. Furthermore, it has also been shown that viral populations exposed to subinhibitory concentrations of the antiviral amiR speed up this process. In this article, we have characterized the molecular evolutionary dynamics of an amiR target sequence in a viral genome under both conditions. The use of Illumina ultradeep sequencing has allowed us to identify virus sequence variants at frequencies as low as 2 x 10 –6 and to track their variation in time before and after the viral population was able of successfully infecting plants fully resistant to the ancestral virus. We found that every site in the amiR-target sequence of the viral genome presented variation and that the variant that eventually broke resistance was sampled among the many coexisting ones. In this system, viral evolution in fully susceptible plants results from an equilibrium between mutation and genetic drift, whereas evolution in partially resistant plants originates from more complex dynamics involving mutation, selection, and drift.
    Print ISSN: 0737-4038
    Electronic ISSN: 1537-1719
    Topics: Biology
    Published by Oxford University Press
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