ArticleBiochemical and biophysical research communications2007
A nucleosome positioned by alpha2/Mcm1 prevents Hap1 activator binding in vivo.
Article in Biochemical and biophysical research communications, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Telomeric repeats act as nucleosome-disfavouring sequences in vivo.Nucleic acids research · 2014Article
- The Cyc8-Tup1 complex inhibits transcription primarily by masking the activation domain of the recruiting protein.Genes & development · 2011Article
- Nucleosome-coupled expression differences in closely-related species.BMC genomics · 2011Article
- Nucleosome-depleted regions in cell-cycle-regulated promoters ensure reliable gene expression in every cell cycle.Developmental cell · 2010Article
- Role of the cell wall integrity and filamentous growth mitogen-activated protein kinase pathways in cell wall remodeling during filamentous growth.Eukaryotic cell · 2009Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Nucleosome positioning has been proposed as a mechanism of transcriptional repression. Here, we examined whether nucleosome positioning affects activator binding in living yeast cells. We introduced the cognate Hap1 binding site (UAS1) at a location 24-43 bp, 29-48 bp, or 61-80 bp interior to the edge of a nucleosome positioned by alpha2/Mcm1 in yeast minichromosomes. Hap1 binding to the UAS1 was severely inhibited, not only at the pseudo-dyad but also in the peripheral region of the positioned nucleosome in alpha cells, while it was detectable in a cells, in which the nucleosomes were not positioned. Hap1 binding was restored in alpha cells with tup1 or isw2 mutations, which caused the loss of nucleosome positioning. These results support the mechanism in which alpha2/Mcm1-dependent nucleosome positioning has a regulatory function to limit the access of transcription factors.
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