<?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%">Filichkin, Sergei A</style></author><author><style face="normal" font="default" size="100%">Cumbie, Jason S</style></author><author><style face="normal" font="default" size="100%">Dharmawardhana, Palitha</style></author><author><style face="normal" font="default" size="100%">Jaiswal, Pankaj</style></author><author><style face="normal" font="default" size="100%">Chang, Jeff H</style></author><author><style face="normal" font="default" size="100%">Palusa, Saiprasad G</style></author><author><style face="normal" font="default" size="100%">Reddy, A S N</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author><author><style face="normal" font="default" size="100%">Mockler, Todd C</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Environmental stresses modulate abundance and timing of alternatively spliced circadian transcripts in Arabidopsis.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Plant</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol Plant</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Alternative Splicing</style></keyword><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%">Circadian Clocks</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Plant</style></keyword><keyword><style  face="normal" font="default" size="100%">Introns</style></keyword><keyword><style  face="normal" font="default" size="100%">Nonsense Mediated mRNA Decay</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">207-27</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Environmental stresses profoundly altered accumulation of nonsense mRNAs including intron-retaining (IR) transcripts in Arabidopsis. Temporal patterns of stress-induced IR mRNAs were dissected using both oscillating and non-oscillating transcripts. Broad-range thermal cycles triggered a sharp increase in the long IR CCA1 isoforms and altered their phasing to different times of day. Both abiotic and biotic stresses such as drought or Pseudomonas syringae infection induced a similar increase. Thermal stress induced a time delay in accumulation of CCA1 I4Rb transcripts, whereas functional mRNA showed steady oscillations. Our data favor a hypothesis that stress-induced instabilities of the central oscillator can be in part compensated through fluctuations in abundance and out-of-phase oscillations of CCA1 IR transcripts. Taken together, our results support a concept that mRNA abundance can be modulated through altering ratios between functional and nonsense/IR transcripts. SR45 protein specifically bound to the retained CCA1 intron in&amp;nbsp;vitro, suggesting that this splicing factor could be involved in regulation of intron retention. Transcriptomes of nonsense-mediated mRNA decay (NMD)-impaired and heat-stressed plants shared a set of retained introns associated with stress- and defense-inducible transcripts. Constitutive activation of certain stress response networks in an NMD mutant could be linked to disequilibrium between functional and nonsense mRNAs.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</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%">Filichkin, Sergei A</style></author><author><style face="normal" font="default" size="100%">Cumbie, Jason S</style></author><author><style face="normal" font="default" size="100%">Dharmawadhana, J Palitha</style></author><author><style face="normal" font="default" size="100%">Jaiswal, Pankaj</style></author><author><style face="normal" font="default" size="100%">Chang, Jeff H</style></author><author><style face="normal" font="default" size="100%">Palusa, Saiprasad G</style></author><author><style face="normal" font="default" size="100%">Reddy, A S N</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author><author><style face="normal" font="default" size="100%">Mockler, Todd C</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Environmental Stresses Modulate Abundance and Timing of Alternatively Spliced Circadian Transcripts in Arabidopsis.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Plant</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol Plant</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Nov 3</style></date></pub-dates></dates><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Environmental stresses profoundly altered accumulation of nonsense mRNAs including intron retaining (IR) transcripts in Arabidopsis. Temporal patterns of stress-induced IR mRNAs were dissected using both oscillating and non-oscillating transcripts. Broad range thermal cycles triggered a sharp increase in the long intron retaining CCA1 isoforms and altered their phasing to different times of day. Both abiotic and biotic stresses such as drought or P. syringae infection induced similar increase. Thermal stress induced a time delay in accumulation of CCA1 I4Rb transcripts whereas functional mRNA showed steady oscillations. Our data favor a hypothesis that stress-induced instabilities of the central oscillator can be in part compensated through fluctuations in abundance and out of phase oscillations of CCA1 IR transcripts. Altogether, our results support a concept that mRNA abundance can be modulated through altering ratios between functional and nonsense/IR transcripts. SR45 protein specifically bound to the retained CCA1 intron in vitro, suggesting that this splicing factor could be involved in regulation of intron retention. Transcriptomes of NMD-impaired and heat-stressed plants shared a set of retained introns associated with stress- and defense-inducible transcripts. Constitutive activation of certain stress response networks in an NMD mutant could be linked to disequilibrium between functional and nonsense mRNAs.&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></records></xml>