RPCC analysis of rap1-sil, tpk1 & tpk2.
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE14077 | GEO | 2009/08/24
SECONDARY ACCESSION(S): PRJNA114625
REPOSITORIES: GEO
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Project description:GRO (Genomic run-on) experiments with different mutants that affect to the accumulation of non active RNA pol II along the yeast genome. Keywords: Genomic run-on GRO
2009-08-24 | GSE14080 | GEO
Project description:RPCC (RNA pol II ChIP-on-chip) experiments with different mutants that affect to the accumulation of non active RNA pol II along the yeast genome. Keywords: ChIP-chip There are 4 different strains: rap1-sil (without the silencing domain), RAP1 (both from Graham I.R. et al 1999) and tpk1 & tpk2 mutants (Euroscarf). The IP was done using an Ab against the RNApol II CTD (8WG16 Covance).There are 3 independent biological replicates of Rap1 and rap1-sil experiments and 2 for the tpk1 & tpk2 experiments.
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Project description:GRO (Genomic run-on) experiments with different mutants that affect to the accumulation of non active RNA pol II along the yeast genome. Keywords: Genomic run-on GRO There are 4 different strains: rap1-sil (without the silencing domain), RAP1(both from Graham I.R. et al 1999) and tpk1 & tpk2 mutants (Euroscarf). For each experiment there are GRO data (Transcription Rate) and gDNA data used for normalizing the GRO signals. The last number of the GRO filters correspond to the number of gDNA filters.There are 3 independent biological replicates of Rap1 and rap1-sil experiments and 2 for the tpk1 & tpk2 experiments.
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Project description:RNA Polymerase II (Pol II) transcriptional recycling is an underappreciated mechanism for which the required factors and contributions to overall gene expression levels are poorly understood. We describe an in vitro methodology facilitating unbiased identification of putative RNA Pol II transcriptional recycling factors and quantitative measurement of transcriptional output from recycled transcriptional components. By combing our in vitro transcription assays with other experiments (e.g. in vivo dynamic ChIP-seq assays), we identified PAF1 complex components and phospho-MED1 as drivers for transcription recycling, revealing a new layer in controlling Pol II-dependent transcription. Our findings also point to RNA Pol II transcription recycling as a mechanism that functions aberrantly in disease states such as cancer, and indicate the potential to target factors such as PAF1 and phospho-MED1 that drive RNA Pol II recycling in cancer.
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