ArticleNucleic acids research2016
RNA Polymerase I and Fob1 contributions to transcriptional silencing at the yeast rDNA locus.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Smc5/6 in the rDNA modulates lifespan independently of Fob1.Aging cell · 2021Article
- Existence, Transition, and Propagation of Intermediate Silencing States in Ribosomal DNA.Molecular and cellular biology · 2019Article
- Endogenous single-strand DNA breaks at RNA polymerase II promoters in Saccharomyces cerevisiae.Nucleic acids research · 2018Article
- The Nuts and Bolts of Transcriptionally Silent Chromatin in Saccharomyces cerevisiae.Genetics · 2016Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
RNA polymerase II (Pol II)-transcribed genes embedded within the yeast rDNA locus are repressed through a Sir2-dependent process called 'rDNA silencing'. Sir2 is recruited to the rDNA promoter through interactions with RNA polymerase I (Pol I), and to a pair of DNA replication fork block sites (Ter1 and Ter2) through interaction with Fob1. We utilized a reporter gene (mURA3) integrated adjacent to the leftmost rDNA gene to investigate localized Pol I and Fob1 functions in silencing. Silencing was attenuated by loss of Pol I subunits or insertion of an ectopic Pol I terminator within the adjacent rDNA gene. Silencing left of the rDNA array is naturally attenuated by the presence of only one intact Fob1 binding site (Ter2). Repair of the 2nd Fob1 binding site (Ter1) dramatically strengthens silencing such that it is no longer impacted by local Pol I transcription defects. Global loss of Pol I activity, however, negatively affects Fob1 association with the rDNA. Loss of Ter2 almost completely eliminates localized silencing, but is restored by artificially targeting Fob1 or Sir2 as Gal4 DNA binding domain fusions. We conclude that Fob1 and Pol I make independent contributions to establishment of silencing, though Pol I also reinforces Fob1-dependent silencing.
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Registered trials
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