ArticleMolecular and cellular biology2010
Novel functional residues in the core domain of histone H2B regulate yeast gene expression and silencing and affect the response to DNA damage.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.International journal of molecular sciences · 2024Review
- N-Terminal Tails of Histones H2A and H2B Differentially Affect Transcription by RNA Polymerase II In Vitro.Cells · 2022Article
- Distinct Histone Post-translational Modifications duringJournal of proteome research · 2022Article
- Systematic genetic and proteomic screens during gametogenesis identify H2BK34 methylation as an evolutionary conserved meiotic mark.Epigenetics & chromatin · 2020Article
- The impact of histone post-translational modifications in neurodegenerative diseases.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Epigenetics in amyotrophic lateral sclerosis: a role for histone post-translational modifications in neurodegenerative disease.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Downregulation of Nuclear Protein H2B Induces Salicylic Acid Mediated Defense Against PVX Infection inFrontiers in microbiology · 2019Article
- Neurodegenerative Disease Proteinopathies Are Connected to Distinct Histone Post-translational Modification Landscapes.ACS chemical neuroscience · 2018Article
- Dissecting Nucleosome Function with a Comprehensive Histone H2A and H2B Mutant Library.G3 (Bethesda, Md.) · 2017Article
- A basic domain in the histone H2B N-terminal tail is important for nucleosome assembly by FACT.Nucleic acids research · 2016Article
- Histone Sprocket Arginine Residues Are Important for Gene Expression, DNA Repair, and Cell Viability in Saccharomyces cerevisiae.Genetics · 2015Article
- Canonical histone H2Ba and H2A.X dimerize in an opposite genomic localization to H2A.Z/H2B.Z dimers in Toxoplasma gondii.Molecular and biochemical parasitology · 2014Article
- Ascending the nucleosome face: recognition and function of structured domains in the histone H2A-H2B dimer.Biochimica et biophysica acta · 2012Article
- Structural basis of silencing: Sir3 BAH domain in complex with a nucleosome at 3.0 Å resolution.Science (New York, N.Y.) · 2011Article
- A region of the nucleosome required for multiple types of transcriptional silencing in Saccharomyces cerevisiae.Genetics · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies have identified novel modifications in the core fold domain of histone H2B, but relatively little is known about the function of these putative histone modification sites. We have mutated core modifiable residues that are conserved in Saccharomyces cerevisiae histone H2B and characterized the effects of the mutants on yeast silencing, gene expression, and the DNA damage response. We identified three histone H2B core modifiable residues as functionally important. We find that mutating H2B K49 in yeast confers a UV sensitivity phenotype, and we confirm that the homologous residue in human histone H2B is acetylated and methylated in human cells. Our results also indicate that mutating H2B K111 impairs the response to methyl methanesulfonate (MMS)-induced DNA lesions and disrupts telomeric silencing and Sir4 binding. In contrast, mutating H2B R102 enhances silencing at yeast telomeres and the HML silent mating loci and increases Sir4 binding to these regions. The H2B R102A mutant also represses the expression of endogenous genes adjacent to yeast telomeres, which is likely due to the ectopic spreading of the Sir complex in this mutant strain. We propose a structural model by which H2B R102 and K111 regulate the binding of the Sir complex to the nucleosome.
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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.