ArticleNucleic acids research2004
Repression of the yeast HO gene by the MATalpha2 and MATa1 homeodomain proteins.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 19 citations in OpenAlex.
- Amn1 governs post-mitotic cell separation in Saccharomyces cerevisiae.PLoS genetics · 2018Article
- Construction of hybrid regulated mother-specific yeast promoters for inducible differential gene expression.PloS one · 2018Article
- Disruption of promoter memory by synthesis of a long noncoding RNA.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Chimeric Sex-Determining Chromosomal Regions and Dysregulation of Cell-Type Identity in a Sterile Zygosaccharomyces Allodiploid Yeast.PloS one · 2016Article
- Article
- Dancing the cell cycle two-step: regulation of yeast G1-cell-cycle genes by chromatin structure.Trends in biochemical sciences · 2013Review
- Quality control of MATa1 splicing and exon skipping by nuclear RNA degradation.Nucleic acids research · 2012Article
- Regulated antisense transcription controls expression of cell-type-specific genes in yeast.Molecular and cellular biology · 2011Article
- Fungal sex and pathogenesis.Clinical microbiology reviews · 2010Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The HO gene in Saccharomyces cerevisiae is regulated by a large and complex promoter that is similar to promoters in higher order eukaryotes. Within this promoter are 10 potential binding sites for the a1-alpha2 heterodimer, which represses HO and other haploid-specific genes in diploid yeast cells. We have determined that a1-alpha2 binds to these sites with differing affinity, and that while certain strong-affinity sites are crucial for repression of HO, some of the weak-affinity sites are dispensable. However, these weak-affinity a1-alpha2-binding sites are strongly conserved in related yeast species and have a role in maintaining repression upon the loss of strong-affinity sites. We found that these weak sites are sufficient for a1-alpha2 to partially repress HO and recruit the Tup1-Cyc8 (Tup1-Ssn6) co-repressor complex to the HO promoter. We demonstrate that the Swi5 activator protein is not bound to URS1 in diploid cells, suggesting that recruitment of the Tup1-Cyc8 complex by a1-alpha2 prevents DNA binding by activator proteins resulting in repression of HO.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.