Interaction of RNA polymerase II and the RNA silencing machinery in heterochromatin formation of Drosophila

2008 ◽  
Author(s):  
Harsh Kavi
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Rna Silencing ◽  
Heterochromatin Formation

scholarly journals Subunit Compositions of the RNA-Silencing Enzymes Pol IV and Pol V Reveal Their Origins as Specialized Forms of RNA Polymerase II

2009 ◽  
Vol 33 (2) ◽  
pp. 192-203 ◽  
Author(s):  
Thomas S. Ream ◽  
Jeremy R. Haag ◽  
Andrzej T. Wierzbicki ◽  
Carrie D. Nicora ◽  
Angela D. Norbeck ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Rna Silencing ◽  
Pol Iv ◽  
Pol V

Gene insulation. Part I: natural strategies in yeast and Drosophila

2010 ◽  
Vol 88 (6) ◽  
pp. 875-884 ◽  
Author(s):  
Michèle Amouyal
Keyword(s):  
Gene Expression ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Transcription Initiation ◽  
Rna Polymerase Iii ◽  
Eukaryotic Cells ◽  
Trna Genes ◽  
Initiation Complex ◽  
Heterochromatin Formation ◽  
Transcription Initiation Complex

This review in two parts deals with the increasing number of processes known to be used by eukaryotic cells to protect gene expression from undesired genomic enhancer or chromatin effects, by means of the so-called insulators or barriers. The most advanced studies in this expanding field concern yeasts and Drosophila (this article) and the vertebrates (next article in this issue). Clearly, the cell makes use of every gene context to find the appropriate, economic, solution. Thus, besides the elements formerly identified and specifically dedicated to insulation, a number of unexpected elements are diverted from their usual function to structure the genome and enhancer action or to prevent heterochromatin spreading. They are, for instance, genes actively transcribed by RNA polymerase II or III, partial elements of these transcriptional machineries (stalled RNA polymerase II, normally required by genes that must respond quickly to stimuli, or TFIIIC bound at its B-box, normally required by RNA polymerase III for assembly of the transcription initiation complex at tRNA genes), or genomic sequences occupied by variants of standard histones, which, being rapidly and permanently replaced, impede heterochromatin formation.

scholarly journals Piwi suppresses transcription of Brahma-dependent transposons via Maelstrom in ovarian somatic cells

2020 ◽  
Vol 6 (50) ◽  
pp. eaaz7420
Author(s):  
Ryo Onishi ◽  
Kaoru Sato ◽  
Kensaku Murano ◽  
Lumi Negishi ◽  
Haruhiko Siomi ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Chromatin Remodeling ◽  
Adenosine Triphosphatase ◽  
Somatic Cells ◽  
Pol Ii ◽  
Heterochromatin Formation ◽  
Rna Transcripts ◽  
The Core ◽  
Chromatin Remodeling Complex

Drosophila Piwi associates with PIWI-interacting RNAs (piRNAs) and represses transposons transcriptionally through heterochromatinization; however, this process is poorly understood. Here, we identify Brahma (Brm), the core adenosine triphosphatase of the SWI/SNF chromatin remodeling complex, as a new Piwi interactor, and show Brm involvement in activating transcription of Piwi-targeted transposons before silencing. Bioinformatic analyses indicated that Piwi, once bound to target RNAs, reduced the occupancies of SWI/SNF and RNA polymerase II (Pol II) on target loci, abrogating transcription. Artificial piRNA-driven targeting of Piwi to RNA transcripts enhanced repression of Brm-dependent reporters compared with Brm-independent reporters. This was dependent on Piwi cofactors, Gtsf1/Asterix (Gtsf1), Panoramix/Silencio (Panx), and Maelstrom (Mael), but not Eggless/dSetdb (Egg)–mediated H3K9me3 deposition. The λN-box B–mediated tethering of Mael to reporters repressed Brm-dependent genes in the absence of Piwi, Panx, and Gtsf1. We propose that Piwi, via Mael, can rapidly suppress transcription of Brm-dependent genes to facilitate heterochromatin formation.

scholarly journals TASOR epigenetic repressor cooperates with a CNOT1 RNA degradation pathway to repress HIV

2020 ◽  
Author(s):  
Roy Matkovic ◽  
Marina Morel ◽  
Pauline Larrous ◽  
Benjamin Martin ◽  
Fabienne Bejjani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Rna Degradation ◽  
Degradation Pathway ◽  
Transcriptional Level ◽  
Heterochromatin Formation ◽  
Nascent Transcripts ◽  
Ribosomal Dnas

AbstractThe Human Silencing Hub (HUSH) complex constituted of TASOR, MPP8 and Periphilin is involved in the spreading of H3K9me3 repressive marks across genes and transgenes such as ZNF encoding genes, ribosomal DNAs, LINE-1, Retrotransposons and Retroelements or the integrated HIV provirus1–5. The deposit of these repressive marks leads to heterochromatin formation and inhibits gene expression. The precise mechanisms of silencing mediated by HUSH is still poorly understood. Here, we show that TASOR depletion increases the accumulation of transcripts derived from the HIV-1 LTR promoter at a post-transcriptional level. By counteracting HUSH, Vpx from HIV-2 mimics TASOR depletion. With the use of a Yeast-Two-Hybrid screen, we identified new TASOR partners involved in RNA metabolism including the RNA deadenylase CCR4-NOT complex scaffold CNOT1. TASOR and CNOT1 interact in vivo and synergistically repress HIV expression from its LTR. In fission yeast, the RNA-induced transcriptional silencing (RITS) complex presents structural homology with HUSH. During transcription elongation by RNA polymerase II, RITS recruits a TRAMP-like RNA degradation complex composed of CNOT1 partners, MTR4 and the exosome, to ultimately repress gene expression via H3K9me3 deposit. Similarly, we show that TASOR interacts and cooperates with MTR4 and the exosome, in addition to CNOT1. We also highlight an interaction between TASOR and RNA Polymerase II, predominantly under its elongating state, and between TASOR and some HUSH-targeted nascent transcripts. Furthermore, we show that TASOR overexpression facilitates the association of the aforementioned RNA degradation proteins with RNA polymerase II. Altogether, we propose that HUSH operates at the transcriptional and post-transcriptional levels to repress HIV proviral gene expression.

An atypical RNA polymerase involved in RNA silencing shares small subunits with RNA polymerase II

2008 ◽  
Vol 16 (1) ◽  
pp. 91-93 ◽  
Author(s):  
Linfeng Huang ◽  
Alexandra M E Jones ◽  
Iain Searle ◽  
Kanu Patel ◽  
Hannes Vogler ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Rna Silencing

scholarly journals TASOR epigenetic repressor cooperates with a CNOT1 RNA degradation pathway to repress HIV

2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Roy Matkovic ◽  
Marina Morel ◽  
Sophie Lanciano ◽  
Pauline Larrous ◽  
Benjamin Martin ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Integration Site ◽  
Underlying Mechanism ◽  
Rna Degradation ◽  
Degradation Pathway ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Methyl Transferase ◽  
Heterochromatin Formation

AbstractThe Human Silencing Hub (HUSH) complex constituted of TASOR, MPP8 and Periphilin recruits the histone methyl-transferase SETDB1 to spread H3K9me3 repressive marks across genes and transgenes in an integration site-dependent manner. The deposition of these repressive marks leads to heterochromatin formation and inhibits gene expression, but the underlying mechanism is not fully understood. Here, we show that TASOR silencing or HIV-2 Vpx expression, which induces TASOR degradation, increases the accumulation of transcripts derived from the HIV-1 LTR promoter at a post-transcriptional level. Furthermore, using a yeast 2-hybrid screen, we identify new TASOR partners involved in RNA metabolism including the RNA deadenylase CCR4-NOT complex scaffold CNOT1. TASOR and CNOT1 synergistically repress HIV expression from its LTR. Similar to the RNA-induced transcriptional silencing complex found in fission yeast, we show that TASOR interacts with the RNA exosome and RNA Polymerase II, predominantly under its elongating state. Finally, we show that TASOR facilitates the association of RNA degradation proteins with RNA polymerase II and is detected at transcriptional centers. Altogether, we propose that HUSH operates at the transcriptional and post-transcriptional levels to repress HIV proviral expression.

Nutrient-regulated gene expression in eukaryotes

2006 ◽  
Vol 73 ◽  
pp. 85-96 ◽  
Author(s):  
Richard J. Reece ◽  
Laila Beynon ◽  
Stacey Holden ◽  
Amanda D. Hughes ◽  
Karine Rébora ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Transcriptional Control ◽  
Direct Interaction ◽  
Signalling Pathways ◽  
A Cell ◽  
One Step ◽  
Higher Eukaryotes ◽  
Regulated Gene Expression

The recognition of changes in environmental conditions, and the ability to adapt to these changes, is essential for the viability of cells. There are numerous well characterized systems by which the presence or absence of an individual metabolite may be recognized by a cell. However, the recognition of a metabolite is just one step in a process that often results in changes in the expression of whole sets of genes required to respond to that metabolite. In higher eukaryotes, the signalling pathway between metabolite recognition and transcriptional control can be complex. Recent evidence from the relatively simple eukaryote yeast suggests that complex signalling pathways may be circumvented through the direct interaction between individual metabolites and regulators of RNA polymerase II-mediated transcription. Biochemical and structural analyses are beginning to unravel these elegant genetic control elements.

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