ArticlePLoS genetics2008
Compensatory interactions between Sir3p and the nucleosomal LRS surface imply their direct interaction.
Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Histone 3.3-related chromatinopathy: missense variants throughout H3-3A and H3-3B cause a range of functional consequences across species.Human genetics · 2024Review
- Systematic histone H4 replacement in Arabidopsis thaliana reveals a role for H4R17 in regulating flowering time.The Plant cell · 2022Article
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- Histone H3.3 beyond cancer: Germline mutations inScience advances · 2020Article
- Systematic genetic and proteomic screens during gametogenesis identify H2BK34 methylation as an evolutionary conserved meiotic mark.Epigenetics & chromatin · 2020Article
- Histone H3E73Q and H4E53A mutations cause recombinogenic DNA damage.Microbial cell (Graz, Austria) · 2020Article
- Structure and function of the Orc1 BAH-nucleosome complex.Nature communications · 2019Article
- Yeast heterochromatin regulators Sir2 and Sir3 act directly at euchromatic DNA replication origins.PLoS genetics · 2018Article
- Dissecting Nucleosome Function with a Comprehensive Histone H2A and H2B Mutant Library.G3 (Bethesda, Md.) · 2017Article
- The Nuts and Bolts of Transcriptionally Silent Chromatin in Saccharomyces cerevisiae.Genetics · 2016Review
- Review
- Nucleosome structure and function.Chemical reviews · 2015Review
- The BAH domain of Rsc2 is a histone H3 binding domain.Nucleic acids research · 2013Article
- Heterochromatin protein Sir3 induces contacts between the amino terminus of histone H4 and nucleosomal DNA.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The role of the nucleosome acidic patch in modulating higher order chromatin structure.Journal of the Royal Society, Interface · 2013Review
- Ascending the nucleosome face: recognition and function of structured domains in the histone H2A-H2B dimer.Biochimica et biophysica acta · 2012Article
- Functions of protosilencers in the formation and maintenance of heterochromatin in Saccharomyces cerevisiae.PloS one · 2012Article
- Structural basis of silencing: Sir3 BAH domain in complex with a nucleosome at 3.0 Å resolution.Science (New York, N.Y.) · 2011Article
- Structural basis for the role of the Sir3 AAA+ domain in silencing: interaction with Sir4 and unmethylated histone H3K79.Genes & development · 2011Article
- A region of the nucleosome required for multiple types of transcriptional silencing in Saccharomyces cerevisiae.Genetics · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The previously identified LRS (Loss of rDNA Silencing) domain of the nucleosome is critically important for silencing at both ribosomal DNA and telomeres. To understand the function of the LRS surface in silencing, we performed an EMS mutagenesis screen to identify suppressors of the H3 A75V LRS allele. We identified dominant and recessive mutations in histones H3, H4, and dominant mutations in the BAH (Bromo Adjacent Homology) domain of SIR3. We further characterized a surface of Sir3p critical for silencing via the LRS surface. We found that all alleles of the SIR3 BAH domain were able to 1) generally suppress the loss of telomeric silencing of LRS alleles, but 2) could not suppress SIN (Swi/Snf Independent) alleles or 3) could not suppress the telomeric silencing defect of H4 tail alleles. Moreover, we noticed a complementary trend in the electrostatic changes resulting from most of the histone mutations that gain or lose silencing and the suppressor alleles isolated in SIR3, and the genes for histones H3 and H4. Mutations in H3 and H4 genes that lose silencing tend to make the LRS surface more electronegative, whereas mutations that increase silencing make it less electronegative. Conversely, suppressors of LRS alleles in either SIR3, histone H3, or H4 also tend to make their respective surfaces less electronegative. Our results provide genetic evidence for recent data suggesting that the Sir3p BAH domain directly binds the LRS domain. Based on these findings, we propose an electrostatic model for how an extensive surface on the Sir3p BAH domain may regulate docking onto the LRS surface.
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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.