Pol III ChIP-seq mouse development
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Claudia Kutter
PROVIDER: E-MTAB-2326 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The genetic code is an abstraction of how mRNA codons and tRNA anticodons molecularly interact during protein synthesis; the stability and regulation of this interaction remains largely unexplored. Here, we quantitatively characterized the expression of mRNA and tRNA genes across developing mouse tissues. Substantial fractions of both gene sets dynamically change expression from early organogenesis to adult tissues. mRNA codon pools are highly stable over development and reflect the genomic background; in contrast, changes in transcription at specific tRNA genes are coordinated across anticodon families to produce a stable isoacceptor output. During development, the pools of mRNA codons and tRNA anticodons are invariant and highly correlated, revealing a stable molecular interaction interlocking transcription and translation.
2014-08-08 | E-MTAB-2328 | biostudies-arrayexpress
Project description:This dataset has been designed to test whether codons in mRNAs and anticodons in tRNAs vary in order to maximize translation in specific cellular conditions in mammals. Prokaryotes and simple unicellular eukaryotes optimize their translational rates by adjusting the codons in the protein-coding transcriptome to the available pool of anticodons in the tRNA transcriptome. We found no evidence supporting this mechanism in mammals, even when subsets of genes were considered, such as those found in Gene Ontology functional categories or in tissue-specific transcriptional signatures. The simplest explanation accounting for the observed codon distributions in mammals is the variation in GC content of gene categories. GC variation across the mammalian genome is most likely to result from the interplay of genome repair and gene duplication mechanisms, rather than selective pressures caused by codon-driven translational rates. This work is part of experiment series: ChIP-Seq E-MTAB-958 and E-MTAB-2326.
2016-04-18 | E-MTAB-4046 | biostudies-arrayexpress
Project description:This dataset has been designed to test whether codons in mRNAs and anticodons in tRNAs vary in order to maximize translation in specific cellular conditions in mammals. Prokaryotes and simple unicellular eukaryotes optimize their translational rates by adjusting the codons in the protein-coding transcriptome to the available pool of anticodons in the tRNA transcriptome. We found no evidence supporting this mechanism in mammals, even when subsets of genes were considered, such as those found in Gene Ontology functional categories or in tissue-specific transcriptional signatures. The simplest explanation accounting for the observed codon distributions in mammals is the variation in GC content of gene categories. GC variation across the mammalian genome is most likely to result from the interplay of genome repair and gene duplication mechanisms, rather than selective pressures caused by codon-driven translational rates. This work is part of experiment series: ChIP-Seq E-MTAB-23282326.
2016-04-18 | E-MTAB-4052 | biostudies-arrayexpress
Project description:The packaging of the genetic material into chromatin imposes the remodeling of this barrier to allow efficient transcription. RNA polymerase II activity is coupled with several histone modification complexes that enforce remodeling. How RNA polymerase III (Pol III) counteracts the inhibitory effect of chromatin is unknown. We report here a mechanism where RNA Polymerase II (Pol II) transcription is required to prime and maintain nucleosome depletion at Pol III loci and contributes to efficient Pol III recruitment upon re-initiation of growth from stationary phase in Fission yeast. The Pcr1 transcription factor participates in the recruitment of Pol II, which affects local histone occupancy through the associated SAGA complex and a Pol II phospho-S2 CTD / Mst2 pathway. These data expand the central role of Pol II in gene expression beyond mRNA synthesis.
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Project description:Spatiotemporal regulation of gene expression depends on the cooperation of multiple mechanisms, including the functional interaction of promoters with distally located enhancers. Here, we show that, in cortical neurons, a subset of short interspersed nuclear elements (SINEs) located in the proximity of activity-regulated genes bears features of enhancers. Enhancer SINEs (eSINEs) recruit the Pol III cofactor complex TFIIIC in a stimulus-dependent manner and are transcribed by Pol III in response to neuronal depolarization. Characterization of an eSINE located in proximity to the Fos gene (FosRSINE1) indicated that the FosRSINE1-encoded transcript interacts with Pol II at the Fos promoter and mediates Fos relocation to Pol II factories, providing an unprecedented molecular link between Pol III and Pol II transcription. Strikingly, knockdown of the FosRSINE1 transcript induces defects of both cortical radial migration in vivo and activity-dependent dendritogenesis in vitro, demonstrating that FosRSINE1 acts as a strong enhancer of Fos expression in diverse physiological contexts.
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Project description:Epigenetic control is an important aspect of gene regulation. Despite detailed understanding of many examples, the transcription of non-coding RNA genes by RNA polymerase (pol) III is less well characterized. Here we profile the epigenetic features of pol III target genes throughout the human genome. This reveals that the chromatin landscape of pol III-transcribed genes resembles that of pol II templates in many ways, although there are also clear differences. Our analysis also discovered an entirely unexpected phenomenon, namely that pol II co-localizes with the majority of genomic loci that are bound by pol III. Chip-Seq experiments for six samples: Pol III, TFIIIB, TFIIIC, H3K4me3 in HeLa cells and Pol III, S2 phos Pol II in CD4+ cells.
2010-04-25 | E-GEOD-20040 | biostudies-arrayexpress
Project description:BackgroundThe relationship between transcription and the 3D chromatin structure is debated. Multiple studies have shown that transcription affects global Cohesin binding and 3D genome structures. However, several other studies have indicated that inhibited transcription does not alter chromatin conformations.ResultsWe provide the most comprehensive evidence to date to demonstrate that transcription plays a relatively modest role in organizing the local, small-scale chromatin structures in mammalian cells. We show degraded Pol I, Pol II, and Pol III proteins in mESCs cause few or no changes in large-scale 3D chromatin structures, selected RNA polymerases with a high abundance of binding sites or active promoter-associated interactions appear to be relatively more affected after the degradation, transcription inhibition alters local, small loop domains, as indicated by high-resolution chromatin interaction maps, and loops with bound Pol II but without Cohesin or CTCF are identified and found to be largely unchanged after transcription inhibition. Interestingly, Pol II depletion for a longer time significantly affects the chromatin accessibility and Cohesin occupancy, suggesting that RNA polymerases are capable of affecting the 3D genome indirectly. These direct and indirect effects explain the previous inconsistent findings on the influence of transcription inhibition on the 3D genome.ConclusionsWe conclude that Pol I, Pol II, and Pol III loss alters local, small-scale chromatin interactions in mammalian cells, suggesting that the 3D chromatin structures are pre-established and relatively stable.
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Project description:Nuclear pores associate with active protein-coding genes in yeast and have been implicated in transcriptional regulation. Here, we show that in addition to transcriptional regulation, key components of C. elegans nuclear pores are required for processing of a subset of small nucleolar RNAs (snoRNAs) and tRNAs transcribed by RNA Polymerase (Pol) III. Chromatin immunoprecipitation of NPP-13 and NPP-3, two integral nuclear pore components, and importin-M-CM-^_ IMB-1, provides strong evidence that this requirement is direct. All three proteins associate specifically with tRNA and snoRNA genes undergoing Pol III transcription. These pore components bind immediately downstream of the Pol III pre-initiation complex, but are not required for Pol III recruitment. Instead, NPP-13 is required for cleavage of tRNA and snoRNA precursors into mature RNAs, whereas Pol II transcript processing occurs normally. Our data suggest that integral nuclear pore proteins act to coordinate transcription and processing of Pol III transcripts in C. elegans. Genome-wide ChIP-seq and ChIP-chip were performed in mixed-stage C. elegans embryos for nuclear pore proteins NPP-13, NPP-3, IMB-1 and chromatin proteins Pol III (RPC-1), TBP-1, TFC-1 (SFC-1), TFC-4 (TAG-315), and Pol II (AMA-1). For RPC-1 and TBP-1 ChIP-seq, embryos depleted for NPP-13 were also used. Total RNAs from wild-type, NPP-13 RNAi, and IMB-1 RNAi embryos were analyzed by RNA-seq.
2013-09-05 | E-GEOD-42714 | biostudies-arrayexpress
Project description:Nuclear pores associate with active protein-coding genes in yeast and have been implicated in transcriptional regulation. Here, we show that in addition to transcriptional regulation, key components of C. elegans nuclear pores are required for processing of a subset of small nucleolar RNAs (snoRNAs) and tRNAs transcribed by RNA Polymerase (Pol) III. Chromatin immunoprecipitation of NPP-13 and NPP-3, two integral nuclear pore components, and importin-M-CM-^_ IMB-1, provides strong evidence that this requirement is direct. All three proteins associate specifically with tRNA and snoRNA genes undergoing Pol III transcription. These pore components bind immediately downstream of the Pol III pre-initiation complex, but are not required for Pol III recruitment. Instead, NPP-13 is required for cleavage of tRNA and snoRNA precursors into mature RNAs, whereas Pol II transcript processing occurs normally. Our data suggest that integral nuclear pore proteins act to coordinate transcription and processing of Pol III transcripts in C. elegans. Genome-wide ChIP-seq and ChIP-chip were performed in mixed-stage C. elegans embryos for nuclear pore proteins NPP-13, NPP-3, IMB-1 and chromatin proteins Pol III (RPC-1), TBP-1, TFC-1 (SFC-1), TFC-4 (TAG-315), and Pol II (AMA-1). For RPC-1 and TBP-1 ChIP-seq, embryos depleted for NPP-13 were also used. Total RNAs from wild-type, NPP-13 RNAi, and IMB-1 RNAi embryos were analyzed by RNA-seq.
2013-09-05 | E-GEOD-42651 | biostudies-arrayexpress
Project description:RNA polymerase III transcribes many noncoding RNAs (e.g. tRNAs) important for translational capacity and other functions. Here, we localized RNA polymerase III, alternative TFIIIB complexes (BRF1/2) and TFIIIC in HeLa cells, determining the Pol III transcriptome, defining gene classes, and revealing ‘TFIIIC-only’ sites. Pol III localization in other transformed and primary cell lines revealed both novel and cell-type specific Pol III loci, and one occupied miRNA. Surprisingly, only a fraction of the in silico-predicted Pol III loci are occupied. Interestingly, many occupied Pol III genes reside within an annotated Pol II promoter. Outside of Pol II promoters, occupied Pol III genes overlap with enhancer-like chromatin and enhancer binding proteins such as ETS1 and STAT1. Remarkably, Pol III occupancy scales with the levels of nearby Pol II, active chromatin and CpG content. Taken together, active promoter and enhancer-like chromatin appears to gate Pol III accessibility to the genome. Use of ChIP-array to identify genomic regions bound by RNA Polymerase III machinery
2010-04-14 | E-GEOD-20609 | biostudies-arrayexpress