ArticleMolecular and cellular biology2005
Mutations in the nucleosome core enhance transcriptional silencing.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Proliferating cell nuclear antigen (PCNA) contributes to the high-order structure and stability of heterochromatin in Saccharomyces cerevisiae.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2017Article
- Mutations that prevent or mimic persistent post-translational modifications of the histone H3 globular domain cause lethality and growth defects in Drosophila.Epigenetics & chromatin · 2016Article
- Parasite epigenetics and immune evasion: lessons from budding yeast.Epigenetics & chromatin · 2013Article
- Analysis of epigenetic stability and conversions in Saccharomyces cerevisiae reveals a novel role of CAF-I in position-effect variegation.Nucleic acids research · 2013Article
- Functions of protosilencers in the formation and maintenance of heterochromatin in Saccharomyces cerevisiae.PloS one · 2012Article
- Differential contributions of histone H3 and H4 residues to heterochromatin structure.Genetics · 2011Article
- Proliferating cell nuclear antigen (PCNA) is required for cell cycle-regulated silent chromatin on replicated and nonreplicated genes.The Journal of biological chemistry · 2010Article
- Novel functional residues in the core domain of histone H2B regulate yeast gene expression and silencing and affect the response to DNA damage.Molecular and cellular biology · 2010Article
- Saccharomyces cerevisiae Esc2p interacts with Sir2p through a small ubiquitin-like modifier (SUMO)-binding motif and regulates transcriptionally silent chromatin in a locus-dependent manner.The Journal of biological chemistry · 2010Article
- Mutational analysis of the Sir3 BAH domain reveals multiple points of interaction with nucleosomes.Molecular and cellular biology · 2009Article
- Saccharomyces cerevisiae linker histone Hho1p functionally interacts with core histone H4 and negatively regulates the establishment of transcriptionally silent chromatin.The Journal of biological chemistry · 2009Article
- Compensatory interactions between Sir3p and the nucleosomal LRS surface imply their direct interaction.PLoS genetics · 2008Article
- Article
- Cell cycle requirements in assembling silent chromatin in Saccharomyces cerevisiae.Molecular and cellular biology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Transcriptional silencing in Saccharomyces requires specific nucleosome modifications promoted in part by a complex of Sir proteins that binds to the modified nucleosomes. Recent evidence suggests that modifications of both the histone amino termini and the core domain of nucleosomes contribute to silencing. We previously identified histone H4 mutations affecting residues in the core of the nucleosome that yield enhanced silencing at telomeres. Here we show that enhanced silencing induced by these mutations increases the proportion of cells in which telomeres and silent mating-type loci are in the silent state. One H4 mutation affects the expression of a subset of genes whose expression is altered by deletion of HTZ1, which encodes the histone variant H2A.Z, suggesting that the mutation may antagonize H2A.Z incorporation into nucleosomes. A second mutation causes the spread of silencing into subtelomeric regions that are not normally silenced in wild-type cells. Mechanistically, this mutation does not significantly accelerate the formation of silent chromatin but, rather, reduces the rate of decay of the silenced state. We propose that these mutations use distinct mechanisms to affect the dynamic interplay between activation and repression at the boundary between active and silent chromatin.
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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.