<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Colleen Doherty</style></author><author><style face="normal" font="default" size="100%">Joanna Friesner</style></author><author><style face="normal" font="default" size="100%">Brian Gregory</style></author><author><style face="normal" font="default" size="100%">Ann Loraine</style></author><author><style face="normal" font="default" size="100%">Molly Megraw</style></author><author><style face="normal" font="default" size="100%">Nicholas Provart</style></author><author><style face="normal" font="default" size="100%">R Keith Slotkin</style></author><author><style face="normal" font="default" size="100%">Chris Town</style></author><author><style face="normal" font="default" size="100%">Sarah M Assmann</style></author><author><style face="normal" font="default" size="100%">Michael Axtell</style></author><author><style face="normal" font="default" size="100%">Tanya Berardini</style></author><author><style face="normal" font="default" size="100%">Sixue Chen</style></author><author><style face="normal" font="default" size="100%">Malia Gehan</style></author><author><style face="normal" font="default" size="100%">Eva Huala</style></author><author><style face="normal" font="default" size="100%">Pankaj Jaiswal</style></author><author><style face="normal" font="default" size="100%">Stephen Larson</style></author><author><style face="normal" font="default" size="100%">Song Li</style></author><author><style face="normal" font="default" size="100%">Sean May</style></author><author><style face="normal" font="default" size="100%">Todd Michael</style></author><author><style face="normal" font="default" size="100%">Chris Pires</style></author><author><style face="normal" font="default" size="100%">Chris Topp</style></author><author><style face="normal" font="default" size="100%">Justin Walley</style></author><author><style face="normal" font="default" size="100%">Eve Wurtele</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Arabidopsis bioinformatics resources: The current state, challenges, and priorities for the future</style></title><secondary-title><style face="normal" font="default" size="100%">Plant Direct</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/2019</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">https://onlinelibrary.wiley.com/doi/full/10.1002/pld3.109</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">3</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">1</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Joanna Friesner</style></author><author><style face="normal" font="default" size="100%">Sarah M. Assmann</style></author><author><style face="normal" font="default" size="100%">Ruth Bastow</style></author><author><style face="normal" font="default" size="100%">Julia Bailey-Serres</style></author><author><style face="normal" font="default" size="100%">Jim Beynon</style></author><author><style face="normal" font="default" size="100%">Volker Brendel</style></author><author><style face="normal" font="default" size="100%">C. Robin Buell</style></author><author><style face="normal" font="default" size="100%">Alexander Bucksch</style></author><author><style face="normal" font="default" size="100%">Wolfgang Busch</style></author><author><style face="normal" font="default" size="100%">Taku Demura</style></author><author><style face="normal" font="default" size="100%">Jose R. Dinneny</style></author><author><style face="normal" font="default" size="100%">Colleen J. Doherty</style></author><author><style face="normal" font="default" size="100%">Andrea L. Eveland</style></author><author><style face="normal" font="default" size="100%">Pascal Falter-Braun</style></author><author><style face="normal" font="default" size="100%">Malia A. Gehan</style></author><author><style face="normal" font="default" size="100%">Michael Gonzales</style></author><author><style face="normal" font="default" size="100%">Erich Grotewold</style></author><author><style face="normal" font="default" size="100%">Rodrigo Gutierrez</style></author><author><style face="normal" font="default" size="100%">Ute Kramer</style></author><author><style face="normal" font="default" size="100%">Gabriel Krouk</style></author><author><style face="normal" font="default" size="100%">Shisong Ma</style></author><author><style face="normal" font="default" size="100%">R.J. Cody Markelz</style></author><author><style face="normal" font="default" size="100%">Molly Megraw</style></author><author><style face="normal" font="default" size="100%">Blake C. Meyers</style></author><author><style face="normal" font="default" size="100%">James A.H. Murray</style></author><author><style face="normal" font="default" size="100%">Nicholas J. Provart</style></author><author><style face="normal" font="default" size="100%">Sue Rhee</style></author><author><style face="normal" font="default" size="100%">Roger Smith</style></author><author><style face="normal" font="default" size="100%">Edgar P. Spalding</style></author><author><style face="normal" font="default" size="100%">Crispin Taylor</style></author><author><style face="normal" font="default" size="100%">Tracy K. Teal</style></author><author><style face="normal" font="default" size="100%">Keiko U. Torii</style></author><author><style face="normal" font="default" size="100%">Chris Town</style></author><author><style face="normal" font="default" size="100%">Matthew Vaughn</style></author><author><style face="normal" font="default" size="100%">Richard Vierstra</style></author><author><style face="normal" font="default" size="100%">Doreen Ware</style></author><author><style face="normal" font="default" size="100%">Olivia Wilkins</style></author><author><style face="normal" font="default" size="100%">Cranos Williams</style></author><author><style face="normal" font="default" size="100%">Siobhan M. Brady</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The Next Generation of Training for Arabidopsis Researchers: Bioinformatics and Quantitative Biology</style></title><secondary-title><style face="normal" font="default" size="100%">Plant Physiology</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/2017</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.plantphysiol.org/content/175/4/1499</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">175</style></volume><pages><style face="normal" font="default" size="100%">1499-1509</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;div&gt;It has been more than 50 years since Arabidopsis (Arabidopsis thaliana) was first introduced as a model organism to understand basic processes in plant biology. A well-organized scientific community has used this small reference plant species to make numerous fundamental plant biology discoveries (Provart et al., 2016). Due to an extremely well-annotated genome and advances in high-throughput sequencing, our understanding of this organism and other plant species has become even more intricate and complex. Computational resources, including CyVerse,3 Araport,4 The Arabidopsis Information Resource (TAIR),5 and BAR,6 have further facilitated novel findings with just the click of a mouse. As we move toward understanding biological systems, Arabidopsis researchers will need to use more quantitative and computational approaches to extract novel biological findings from these data. Here, we discuss guidelines, skill sets, and core competencies that should be considered when developing curricula or training undergraduate or graduate students, postdoctoral researchers, and faculty. A selected case study provides more specificity as to the concrete issues plant biologists face and how best to address such challenges.&lt;/div&gt;</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Ivanchenko, Maria G</style></author><author><style face="normal" font="default" size="100%">Zhu, Jinsheng</style></author><author><style face="normal" font="default" size="100%">Wang, Bangjun</style></author><author><style face="normal" font="default" size="100%">Medvecká, Eva</style></author><author><style face="normal" font="default" size="100%">Du, Yunlong</style></author><author><style face="normal" font="default" size="100%">Azzarello, Elisa</style></author><author><style face="normal" font="default" size="100%">Mancuso, Stefano</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author><author><style face="normal" font="default" size="100%">Filichkin, Sergei</style></author><author><style face="normal" font="default" size="100%">Dubrovsky, Joseph G</style></author><author><style face="normal" font="default" size="100%">Friml, Jiří</style></author><author><style face="normal" font="default" size="100%">Geisler, Markus</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The cyclophilin A DIAGEOTROPICA gene affects auxin transport in both root and shoot to control lateral root formation.</style></title><secondary-title><style face="normal" font="default" size="100%">Development</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Development</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arabidopsis</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Transport</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyclophilin A</style></keyword><keyword><style  face="normal" font="default" size="100%">Indoleacetic Acids</style></keyword><keyword><style  face="normal" font="default" size="100%">Lycopersicon esculentum</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Roots</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Shoots</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Feb 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">142</style></volume><pages><style face="normal" font="default" size="100%">712-21</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Cyclophilin A is a conserved peptidyl-prolyl cis-trans isomerase (PPIase) best known as the cellular receptor of the immunosuppressant cyclosporine A. Despite significant effort, evidence of developmental functions of cyclophilin A in non-plant systems has remained obscure. Mutations in a tomato (Solanum lycopersicum) cyclophilin A ortholog, DIAGEOTROPICA (DGT), have been shown to abolish the organogenesis of lateral roots; however, a mechanistic explanation of the phenotype is lacking. Here, we show that the dgt mutant lacks auxin maxima relevant to priming and specification of lateral root founder cells. DGT is expressed in shoot and root, and localizes to both the nucleus and cytoplasm during lateral root organogenesis. Mutation of ENTIRE/IAA9, a member of the auxin-responsive Aux/IAA protein family of transcriptional repressors, partially restores the inability of dgt to initiate lateral root primordia but not the primordia outgrowth. By comparison, grafting of a wild-type scion restores the process of lateral root formation, consistent with participation of a mobile signal. Antibodies do not detect movement of the DGT protein into the dgt rootstock; however, experiments with radiolabeled auxin and an auxin-specific microelectrode demonstrate abnormal auxin fluxes. Functional studies of DGT in heterologous yeast and tobacco-leaf auxin-transport systems demonstrate that DGT negatively regulates PIN-FORMED (PIN) auxin efflux transporters by affecting their plasma membrane localization. Studies in tomato support complex effects of the dgt mutation on PIN expression level, expression domain and plasma membrane localization. Our data demonstrate that DGT regulates auxin transport in lateral root formation.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Morton, Taj</style></author><author><style face="normal" font="default" size="100%">Wong, Weng-Keen</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">TIPR: transcription initiation pattern recognition on a genome scale.</style></title><secondary-title><style face="normal" font="default" size="100%">Bioinformatics</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Bioinformatics</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Algorithms</style></keyword><keyword><style  face="normal" font="default" size="100%">Genomics</style></keyword><keyword><style  face="normal" font="default" size="100%">Machine Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Sequence Annotation</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Analysis, DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Software</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Initiation Site</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Initiation, Genetic</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Dec 1</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">31</style></volume><pages><style face="normal" font="default" size="100%">3725-32</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;MOTIVATION: &lt;/b&gt;The computational identification of gene transcription start sites (TSSs) can provide insights into the regulation and function of genes without performing expensive experiments, particularly in organisms with incomplete annotations. High-resolution general-purpose TSS prediction remains a challenging problem, with little recent progress on the identification and differentiation of TSSs which are arranged in different spatial patterns along the chromosome.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;In this work, we present the Transcription Initiation Pattern Recognizer (TIPR), a sequence-based machine learning model that identifies TSSs with high accuracy and resolution for multiple spatial distribution patterns along the genome, including broadly distributed TSS patterns that have previously been difficult to characterize. TIPR predicts not only the locations of TSSs but also the expected spatial initiation pattern each TSS will form along the chromosome-a novel capability for TSS prediction algorithms. As spatial initiation patterns are associated with spatiotemporal expression patterns and gene function, this capability has the potential to improve gene annotations and our understanding of the regulation of transcription initiation. The high nucleotide resolution of this model locates TSSs within 10 nucleotides or less on average.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONTACT: &lt;/b&gt;megrawm@science.oregonstate.edu.&lt;/p&gt;&lt;p&gt;&lt;a href=&quot;http://megraw-dev.cgrb.oregonstate.edu/TIPR&quot;&gt;[Software and Supplementary Materials Link]&lt;/a&gt;&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">23</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Morton, Taj</style></author><author><style face="normal" font="default" size="100%">Petricka, Jalean</style></author><author><style face="normal" font="default" size="100%">Corcoran, David L</style></author><author><style face="normal" font="default" size="100%">Li, Song</style></author><author><style face="normal" font="default" size="100%">Winter, Cara M</style></author><author><style face="normal" font="default" size="100%">Carda, Alexa</style></author><author><style face="normal" font="default" size="100%">Benfey, Philip N</style></author><author><style face="normal" font="default" size="100%">Ohler, Uwe</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Paired-end analysis of transcription start sites in Arabidopsis reveals plant-specific promoter signatures.</style></title><secondary-title><style face="normal" font="default" size="100%">Plant Cell</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Plant Cell</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arabidopsis</style></keyword><keyword><style  face="normal" font="default" size="100%">Arabidopsis Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Binding Sites</style></keyword><keyword><style  face="normal" font="default" size="100%">Cluster Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA, Plant</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Plant</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome, Plant</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Nucleotide Motifs</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Roots</style></keyword><keyword><style  face="normal" font="default" size="100%">Promoter Regions, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Plant</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Analysis, DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Species Specificity</style></keyword><keyword><style  face="normal" font="default" size="100%">TATA Box</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Initiation Site</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">26</style></volume><pages><style face="normal" font="default" size="100%">2746-60</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Understanding plant gene promoter architecture has long been a challenge due to the lack of relevant large-scale data sets and analysis methods. Here, we present a publicly available, large-scale transcription start site (TSS) data set in plants using a high-resolution method for analysis of 5&amp;#39; ends of mRNA transcripts. Our data set is produced using the paired-end analysis of transcription start sites (PEAT) protocol, providing millions of TSS locations from wild-type Columbia-0 Arabidopsis thaliana whole root samples. Using this data set, we grouped TSS reads into &amp;quot;TSS tag clusters&amp;quot; and categorized clusters into three spatial initiation patterns: narrow peak, broad with peak, and weak peak. We then designed a machine learning model that predicts the presence of TSS tag clusters with outstanding sensitivity and specificity for all three initiation patterns. We used this model to analyze the transcription factor binding site content of promoters exhibiting these initiation patterns. In contrast to the canonical notions of TATA-containing and more broad &amp;quot;TATA-less&amp;quot; promoters, the model shows that, in plants, the vast majority of transcription start sites are TATA free and are defined by a large compendium of known DNA sequence binding elements. We present results on the usage of these elements and provide our Plant PEAT Peaks (3PEAT) model that predicts the presence of TSSs directly from sequence.&lt;/p&gt;&lt;p&gt;&lt;a href=&quot;http://megraw-dev.cgrb.oregonstate.edu/3PEAT&quot;&gt;[Link to Additional Data and Supplementary Materials]&lt;/a&gt;&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">7</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Brady, Siobhan M</style></author><author><style face="normal" font="default" size="100%">Zhang, Lifang</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author><author><style face="normal" font="default" size="100%">Martinez, Natalia J</style></author><author><style face="normal" font="default" size="100%">Jiang, Eric</style></author><author><style face="normal" font="default" size="100%">Yi, Charles S</style></author><author><style face="normal" font="default" size="100%">Liu, Weilin</style></author><author><style face="normal" font="default" size="100%">Zeng, Anna</style></author><author><style face="normal" font="default" size="100%">Taylor-Teeples, Mallorie</style></author><author><style face="normal" font="default" size="100%">Kim, Dahae</style></author><author><style face="normal" font="default" size="100%">Ahnert, Sebastian</style></author><author><style face="normal" font="default" size="100%">Ohler, Uwe</style></author><author><style face="normal" font="default" size="100%">Ware, Doreen</style></author><author><style face="normal" font="default" size="100%">Walhout, Albertha J M</style></author><author><style face="normal" font="default" size="100%">Benfey, Philip N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A stele-enriched gene regulatory network in the Arabidopsis root.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Syst Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol. Syst. Biol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arabidopsis</style></keyword><keyword><style  face="normal" font="default" size="100%">Arabidopsis Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Regulatory Networks</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Roots</style></keyword><keyword><style  face="normal" font="default" size="100%">Reproducibility of Results</style></keyword><keyword><style  face="normal" font="default" size="100%">Systems Biology</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Two-Hybrid System Techniques</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Jan 18</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">7</style></volume><pages><style face="normal" font="default" size="100%">459</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Tightly controlled gene expression is a hallmark of multicellular development and is accomplished by transcription factors (TFs) and microRNAs (miRNAs). Although many studies have focused on identifying downstream targets of these molecules, less is known about the factors that regulate their differential expression. We used data from high spatial resolution gene expression experiments and yeast one-hybrid (Y1H) and two-hybrid (Y2H) assays to delineate a subset of interactions occurring within a gene regulatory network (GRN) that determines tissue-specific TF and miRNA expression in plants. We find that upstream TFs are expressed in more diverse cell types than their targets and that promoters that are bound by a relatively large number of TFs correspond to key developmental regulators. The regulatory consequence of many TFs for their target was experimentally determined using genetic analysis. Remarkably, molecular phenotypes were identified for 65% of the TFs, but morphological phenotypes were associated with only 16%. This indicates that the GRN is robust, and that gene expression changes may be canalized or buffered.&lt;/p&gt;</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Iizasa, Hisashi</style></author><author><style face="normal" font="default" size="100%">Wulff, Bjorn-Erik</style></author><author><style face="normal" font="default" size="100%">Alla, Nageswara R</style></author><author><style face="normal" font="default" size="100%">Maragkakis, Manolis</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author><author><style face="normal" font="default" size="100%">Hatzigeorgiou, Artemis</style></author><author><style face="normal" font="default" size="100%">Iwakiri, Dai</style></author><author><style face="normal" font="default" size="100%">Takada, Kenzo</style></author><author><style face="normal" font="default" size="100%">Wiedmer, Andreas</style></author><author><style face="normal" font="default" size="100%">Showe, Louise</style></author><author><style face="normal" font="default" size="100%">Lieberman, Paul</style></author><author><style face="normal" font="default" size="100%">Nishikura, Kazuko</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Editing of Epstein-Barr virus-encoded BART6 microRNAs controls their dicer targeting and consequently affects viral latency.</style></title><secondary-title><style face="normal" font="default" size="100%">J Biol Chem</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Biol. Chem.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cell Line, Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Epstein-Barr Virus Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Epstein-Barr Virus Nuclear Antigens</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Silencing</style></keyword><keyword><style  face="normal" font="default" size="100%">Herpesvirus 4, Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immediate-Early Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Ribonuclease III</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA Editing</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Trans-Activators</style></keyword><keyword><style  face="normal" font="default" size="100%">Viral Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Virus Latency</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Oct 22</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">285</style></volume><pages><style face="normal" font="default" size="100%">33358-70</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Certain primary transcripts of miRNA (pri-microRNAs) undergo RNA editing that converts adenosine to inosine. The Epstein-Barr virus (EBV) genome encodes multiple microRNA genes of its own. Here we report that primary transcripts of ebv-miR-BART6 (pri-miR-BART6) are edited in latently EBV-infected cells. Editing of wild-type pri-miR-BART6 RNAs dramatically reduced loading of miR-BART6-5p RNAs onto the microRNA-induced silencing complex. Editing of a mutation-containing pri-miR-BART6 found in Daudi Burkitt lymphoma and nasopharyngeal carcinoma C666-1 cell lines suppressed processing of miR-BART6 RNAs. Most importantly, miR-BART6-5p RNAs silence Dicer through multiple target sites located in the 3&amp;#39;-UTR of Dicer mRNA. The significance of miR-BART6 was further investigated in cells in various stages of latency. We found that miR-BART6-5p RNAs suppress the EBNA2 viral oncogene required for transition from immunologically less responsive type I and type II latency to the more immunoreactive type III latency as well as Zta and Rta viral proteins essential for lytic replication, revealing the regulatory function of miR-BART6 in EBV infection and latency. Mutation and A-to-I editing appear to be adaptive mechanisms that antagonize miR-BART6 activities.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">43</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zhang, Lin</style></author><author><style face="normal" font="default" size="100%">Volinia, Stefano</style></author><author><style face="normal" font="default" size="100%">Bonome, Tomas</style></author><author><style face="normal" font="default" size="100%">Calin, George Adrian</style></author><author><style face="normal" font="default" size="100%">Greshock, Joel</style></author><author><style face="normal" font="default" size="100%">Yang, Nuo</style></author><author><style face="normal" font="default" size="100%">Liu, Chang-Gong</style></author><author><style face="normal" font="default" size="100%">Giannakakis, Antonis</style></author><author><style face="normal" font="default" size="100%">Alexiou, Pangiotis</style></author><author><style face="normal" font="default" size="100%">Hasegawa, Kosei</style></author><author><style face="normal" font="default" size="100%">Johnstone, Cameron N</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly S</style></author><author><style face="normal" font="default" size="100%">Adams, Sarah</style></author><author><style face="normal" font="default" size="100%">Lassus, Heini</style></author><author><style face="normal" font="default" size="100%">Huang, Jia</style></author><author><style face="normal" font="default" size="100%">Kaur, Sippy</style></author><author><style face="normal" font="default" size="100%">Liang, Shun</style></author><author><style face="normal" font="default" size="100%">Sethupathy, Praveen</style></author><author><style face="normal" font="default" size="100%">Leminen, Arto</style></author><author><style face="normal" font="default" size="100%">Simossis, Victor A</style></author><author><style face="normal" font="default" size="100%">Sandaltzopoulos, Raphael</style></author><author><style face="normal" font="default" size="100%">Naomoto, Yoshio</style></author><author><style face="normal" font="default" size="100%">Katsaros, Dionyssios</style></author><author><style face="normal" font="default" size="100%">Gimotty, Phyllis A</style></author><author><style face="normal" font="default" size="100%">DeMichele, Angela</style></author><author><style face="normal" font="default" size="100%">Huang, Qihong</style></author><author><style face="normal" font="default" size="100%">Bützow, Ralf</style></author><author><style face="normal" font="default" size="100%">Rustgi, Anil K</style></author><author><style face="normal" font="default" size="100%">Weber, Barbara L</style></author><author><style face="normal" font="default" size="100%">Birrer, Michael J</style></author><author><style face="normal" font="default" size="100%">Hatzigeorgiou, Artemis G</style></author><author><style face="normal" font="default" size="100%">Croce, Carlo M</style></author><author><style face="normal" font="default" size="100%">Coukos, George</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Genomic and epigenetic alterations deregulate microRNA expression in human epithelial ovarian cancer.</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Proc. Natl. Acad. Sci. U.S.A.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">DNA, Neoplasm</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Epigenesis, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Epithelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Neoplastic</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome, Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm Staging</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovarian Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Ribonuclease III</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">Survival Analysis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008 May 13</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">105</style></volume><pages><style face="normal" font="default" size="100%">7004-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;MicroRNAs (miRNAs) are an abundant class of small noncoding RNAs that function as negative gene regulators. miRNA deregulation is involved in the initiation and progression of human cancer; however, the underlying mechanism and its contributions to genome-wide transcriptional changes in cancer are still largely unknown. We studied miRNA deregulation in human epithelial ovarian cancer by integrative genomic approach, including miRNA microarray (n = 106), array-based comparative genomic hybridization (n = 109), cDNA microarray (n = 76), and tissue array (n = 504). miRNA expression is markedly down-regulated in malignant transformation and tumor progression. Genomic copy number loss and epigenetic silencing, respectively, may account for the down-regulation of approximately 15% and at least approximately 36% of miRNAs in advanced ovarian tumors and miRNA down-regulation contributes to a genome-wide transcriptional deregulation. Last, eight miRNAs located in the chromosome 14 miRNA cluster (Dlk1-Gtl2 domain) were identified as potential tumor suppressor genes. Therefore, our results suggest that miRNAs may offer new biomarkers and therapeutic targets in epithelial ovarian cancer.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">19</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zhang, Lin</style></author><author><style face="normal" font="default" size="100%">Huang, Jia</style></author><author><style face="normal" font="default" size="100%">Yang, Nuo</style></author><author><style face="normal" font="default" size="100%">Greshock, Joel</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly S</style></author><author><style face="normal" font="default" size="100%">Giannakakis, Antonis</style></author><author><style face="normal" font="default" size="100%">Liang, Shun</style></author><author><style face="normal" font="default" size="100%">Naylor, Tara L</style></author><author><style face="normal" font="default" size="100%">Barchetti, Andrea</style></author><author><style face="normal" font="default" size="100%">Ward, Michelle R</style></author><author><style face="normal" font="default" size="100%">Yao, George</style></author><author><style face="normal" font="default" size="100%">Medina, Angelica</style></author><author><style face="normal" font="default" size="100%">O'brien-Jenkins, Ann</style></author><author><style face="normal" font="default" size="100%">Katsaros, Dionyssios</style></author><author><style face="normal" font="default" size="100%">Hatzigeorgiou, Artemis</style></author><author><style face="normal" font="default" size="100%">Gimotty, Phyllis A</style></author><author><style face="normal" font="default" size="100%">Weber, Barbara L</style></author><author><style face="normal" font="default" size="100%">Coukos, George</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">microRNAs exhibit high frequency genomic alterations in human cancer.</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Proc. Natl. Acad. Sci. U.S.A.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Breast Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Dosage</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Nucleic Acid Hybridization</style></keyword><keyword><style  face="normal" font="default" size="100%">Oligonucleotide Array Sequence Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovarian Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Statistics as Topic</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2006 Jun 13</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">103</style></volume><pages><style face="normal" font="default" size="100%">9136-41</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;MicroRNAs (miRNAs) are endogenous noncoding RNAs, which negatively regulate gene expression. To determine genomewide miRNA DNA copy number abnormalities in cancer, 283 known human miRNA genes were analyzed by high-resolution array-based comparative genomic hybridization in 227 human ovarian cancer, breast cancer, and melanoma specimens. A high proportion of genomic loci containing miRNA genes exhibited DNA copy number alterations in ovarian cancer (37.1%), breast cancer (72.8%), and melanoma (85.9%), where copy number alterations observed in &amp;gt;15% tumors were considered significant for each miRNA gene. We identified 41 miRNA genes with gene copy number changes that were shared among the three cancer types (26 with gains and 15 with losses) as well as miRNA genes with copy number changes that were unique to each tumor type. Importantly, we show that miRNA copy changes correlate with miRNA expression. Finally, we identified high frequency copy number abnormalities of Dicer1, Argonaute2, and other miRNA-associated genes in breast and ovarian cancer as well as melanoma. These findings support the notion that copy number alterations of miRNAs and their regulatory genes are highly prevalent in cancer and may account partly for the frequent miRNA gene deregulation reported in several tumor types.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">24</style></issue></record></records></xml>