@article {742, title = {Establishment of Expression in the SHORTROOT-SCARECROW Transcriptional Cascade through Opposing Activities of Both Activators and Repressors}, journal = {Dev Cell}, volume = {39}, year = {2016}, month = {12/2016}, pages = {585-596}, abstract = {

Tissue-specific gene expression is often thought to arise from spatially restricted transcriptional cascades. However, it is unclear how expression is established at the top of these cascades in the absence of pre-existing specificity. We generated a transcriptional network to explore how transcription factor expression is established in the Arabidopsis thaliana root ground tissue. Regulators of the SHORTROOT-SCARECROW transcriptional cascade were validated in planta. At the top of this cascade, we identified both activators and repressors of SHORTROOT. The aggregate spatial expression of these regulators is not sufficient to predict transcriptional specificity. Instead, modeling, transcriptional reporters, and synthetic promoters support a mechanism whereby expression at the top of the SHORTROOT-SCARECROW cascade is established through opposing activities of activators and repressors.

}, keywords = {Arabidopsis Proteins/ genetics/ metabolism, Arabidopsis/ genetics/growth \& development/ metabolism, Computer Simulation, Gene Expression Regulation, Plant, Gene Regulatory Networks, Genes, Plant, Genes, Reporter, Genes, Synthetic, Models, Genetic, Plant Roots/cytology/metabolism, Plants, Genetically Modified, Promoter Regions, Genetic, Repressor Proteins/genetics/metabolism, Trans-Activators/genetics/metabolism, Transcription Factors/ genetics/ metabolism, Two-Hybrid System Techniques}, isbn = {1878-1551 (Electronic)1534-5807 (Linking)}, url = {https://doi.org/10.1016/j.devcel.2016.09.031}, author = {Sparks, E. E. and Drapek, C. and Gaudinier, A. and Li, S. and Ansariola, M. and Shen, N. and Hennacy, J. H. and Zhang, J. and Turco, G. and Petricka, J. J. and Foret, J. and Hartemink, A. J. and Gordan, R. and Megraw, M. and Brady, S. M. and Benfey, P. N.} } @article {315, title = {Environmental stresses modulate abundance and timing of alternatively spliced circadian transcripts in Arabidopsis.}, journal = {Mol Plant}, volume = {8}, year = {2015}, month = {2015 Feb}, pages = {207-27}, abstract = {

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\ 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.

}, keywords = {Alternative Splicing, Arabidopsis, Arabidopsis Proteins, Circadian Clocks, Gene Expression Regulation, Plant, Introns, Nonsense Mediated mRNA Decay}, issn = {1752-9867}, doi = {10.1016/j.molp.2014.10.011}, author = {Filichkin, Sergei A and Cumbie, Jason S and Dharmawardhana, Palitha and Jaiswal, Pankaj and Chang, Jeff H and Palusa, Saiprasad G and Reddy, A S N and Megraw, Molly and Mockler, Todd C} } @article {317, title = {Environmental Stresses Modulate Abundance and Timing of Alternatively Spliced Circadian Transcripts in Arabidopsis.}, journal = {Mol Plant}, year = {2014}, month = {2014 Nov 3}, abstract = {

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.

}, issn = {1752-9867}, doi = {10.1093/mp/ssu130}, author = {Filichkin, Sergei A and Cumbie, Jason S and Dharmawadhana, J Palitha and Jaiswal, Pankaj and Chang, Jeff H and Palusa, Saiprasad G and Reddy, A S N and Megraw, Molly and Mockler, Todd C} } @article {323, title = {Editing of Epstein-Barr virus-encoded BART6 microRNAs controls their dicer targeting and consequently affects viral latency.}, journal = {J Biol Chem}, volume = {285}, year = {2010}, month = {2010 Oct 22}, pages = {33358-70}, abstract = {

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\&$\#$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.

}, keywords = {Cell Line, Tumor, Epstein-Barr Virus Infections, Epstein-Barr Virus Nuclear Antigens, Gene Silencing, Herpesvirus 4, Human, Humans, Immediate-Early Proteins, MicroRNAs, Ribonuclease III, RNA Editing, RNA, Viral, Trans-Activators, Viral Proteins, Virus Latency}, issn = {1083-351X}, doi = {10.1074/jbc.M110.138362}, author = {Iizasa, Hisashi and Wulff, Bjorn-Erik and Alla, Nageswara R and Maragkakis, Manolis and Megraw, Molly and Hatzigeorgiou, Artemis and Iwakiri, Dai and Takada, Kenzo and Wiedmer, Andreas and Showe, Louise and Lieberman, Paul and Nishikura, Kazuko} }