Differential regulation of RNA polymerase III genes during liver regeneration

Abstract Mouse liver regeneration after partial hepatectomy involves cells in the remaining tissue synchronously entering the cell division cycle. We have used this system and H3K4me3, Pol II and Pol III profiling to characterize adaptations in Pol III transcription. Our results broadly define a class of genes close to H3K4me3 and Pol II peaks, whose Pol III occupancy is high and stable, and another class, distant from Pol II peaks, whose Pol III occupancy strongly increases after partial hepatectomy. Pol III regulation in the liver thus entails both highly expressed housekeeping genes and genes whose expression can adapt to increased demand.

[1]  Matthew J. Meiners,et al.  Examining the Roles of H3K4 Methylation States with Systematically Characterized Antibodies. , 2018, Molecular cell.

[2]  N. Guex,et al.  Cycles of gene expression and genome response during mammalian tissue regeneration , 2018, Epigenetics & Chromatin.

[3]  R. Roeder,et al.  Regulation of RNA polymerase III transcription during transformation of human IMR90 fibroblasts with defined genetic elements , 2018, Cell cycle.

[4]  N. Guex,et al.  Segregated hepatocyte proliferation and metabolic states within the regenerating mouse liver , 2017, Hepatology communications.

[5]  M. Snyder,et al.  Topological organization and dynamic regulation of human tRNA genes during macrophage differentiation , 2017, Genome Biology.

[6]  V. Praz,et al.  Diurnal regulation of RNA polymerase III transcription is under the control of both the feeding-fasting response and the circadian clock. , 2017, Genome research.

[7]  Henrik Molina,et al.  Modulated Expression of Specific tRNAs Drives Gene Expression and Cancer Progression , 2016, Cell.

[8]  Bianca M. Schmitt,et al.  Codon-Driven Translational Efficiency Is Stable across Diverse Mammalian Cell States , 2016, PLoS genetics.

[9]  V. Praz,et al.  Human MAF1 targets and represses active RNA polymerase III genes by preventing recruitment rather than inducing long-term transcriptional arrest , 2016, Genome research.

[10]  Qi Sun,et al.  Interaction with WDR5 promotes target gene recognition and tumorigenesis by MYC. , 2015, Molecular cell.

[11]  Sebastian M. Waszak,et al.  A Dual Program for Translation Regulation in Cellular Proliferation and Differentiation , 2014, Cell.

[12]  Nuno A. Fonseca,et al.  High-resolution mapping of transcriptional dynamics across tissue development reveals a stable mRNA–tRNA interface , 2014, Genome research.

[13]  Gergana Bounova,et al.  Quantifying ChIP-seq data: a spiking method providing an internal reference for sample-to-sample normalization , 2014 .

[14]  H. Willenbring,et al.  Addendum: A reproducible and well-tolerated method for 2/3 partial hepatectomy in mice , 2014, Nature Protocols.

[15]  B. Cairns,et al.  RNA Polymerase III Transcriptomes in Human Embryonic Stem Cells and Induced Pluripotent Stem Cells, and Relationships with Pluripotency Transcription Factors , 2014, PloS one.

[16]  Michael P Washburn,et al.  Gene duplication and neofunctionalization: POLR3G and POLR3GL , 2014, Genome research.

[17]  N. Guex,et al.  Genome-Wide RNA Polymerase II Profiles and RNA Accumulation Reveal Kinetics of Transcription and Associated Epigenetic Changes During Diurnal Cycles , 2012, PLoS biology.

[18]  V. Praz,et al.  Genomic Study of RNA Polymerase II and III SNAPc-Bound Promoters Reveals a Gene Transcribed by Both Enzymes and a Broad Use of Common Activators , 2012, PLoS genetics.

[19]  M. Delorenzi,et al.  A multiplicity of factors contributes to selective RNA polymerase III occupancy of a subset of RNA polymerase III genes in mouse liver. , 2012, Genome research.

[20]  V. Praz,et al.  Defining the RNA polymerase III transcriptome: Genome-wide localization of the RNA polymerase III transcription machinery in human cells. , 2010, Genome research.

[21]  Peter C. Hollenhorst,et al.  Human RNA Polymerase III transcriptomes and relationships to Pol II promoters, enhancer-binding factors and chromatin domains , 2010, Nature Structural &Molecular Biology.

[22]  Suresh Cuddapah,et al.  Pol II and its associated epigenetic marks are present at pol III-transcribed non-coding RNA genes , 2010, Nature Structural &Molecular Biology.

[23]  Z. Weng,et al.  Genomic Binding Profiles of Functionally Distinct RNA Polymerase III Transcription Complexes in Human Cells , 2010, Nature Structural &Molecular Biology.

[24]  M. Gerstein,et al.  Close association of RNA polymerase II and many transcription factors with Pol III genes , 2010, Proceedings of the National Academy of Sciences.

[25]  T. Pan,et al.  tRNA over-expression in breast cancer and functional consequences , 2009, Nucleic acids research.

[26]  Deborah L. Johnson,et al.  Enhanced RNA Polymerase III-dependent Transcription Is Required for Oncogenic Transformation*♦ , 2008, Journal of Biological Chemistry.

[27]  Korbinian Strimmer,et al.  A unified approach to false discovery rate estimation , 2008, BMC Bioinformatics.

[28]  H. Willenbring,et al.  A reproducible and well-tolerated method for 2/3 partial hepatectomy in mice , 2008, Nature Protocols.

[29]  K. Neugebauer,et al.  Extragenic Accumulation of RNA Polymerase II Enhances Transcription by RNA Polymerase III , 2007, PLoS genetics.

[30]  Robert J. White,et al.  RNA polymerases I and III, growth control and cancer , 2005, Nature Reviews Molecular Cell Biology.

[31]  Robert J White RNA polymerase III transcription and cancer , 2004, Oncogene.

[32]  Gordon K Smyth,et al.  Statistical Applications in Genetics and Molecular Biology Linear Models and Empirical Bayes Methods for Assessing Differential Expression in Microarray Experiments , 2011 .

[33]  John D. Storey,et al.  Statistical significance for genomewide studies , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[34]  R. Eisenman,et al.  Direct activation of RNA polymerase III transcription by c-Myc , 2003, Nature.