ArticleMolecular and cellular biology2011
Key functional regions in the histone variant H2A.Z C-terminal docking domain.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Cancer histone H2A.Z missense mutations disrupt function through distinct local and allosteric effects.Research square · 2026Article
- Characterizing the regulatory effects of H2A.Z and SWR1-C on gene expression during hydroxyurea exposure in Saccharomyces cerevisiae.PLoS genetics · 2025Article
- Epigenetic modulation via the C-terminal tail of H2A.Z.Nature communications · 2024Article
- Article
- What makes a histone variant a variant: Changing H2A to become H2A.Z.PLoS genetics · 2021Article
- Structural basis of chromatin regulation by histone variant H2A.Z.Nucleic acids research · 2021Article
- Structural basis of nucleosome dynamics modulation by histone variants H2A.B and H2A.Z.2.2.The EMBO journal · 2021Article
- MacroH2A1 chromatin specification requires its docking domain and acetylation of H2B lysine 20.Nature communications · 2018Article
- The Swr1 chromatin-remodeling complex prevents genome instability induced by replication fork progression defects.Nature communications · 2018Article
- SMYD3 Promotes Homologous Recombination via Regulation of H3K4-mediated Gene Expression.Scientific reports · 2017Article
- Regulation of Budding Yeast CENP-A levels Prevents Misincorporation at Promoter Nucleosomes and Transcriptional Defects.PLoS genetics · 2016Article
- High-resolution network biology: connecting sequence with function.Nature reviews. Genetics · 2013Review
- Unexplored potentials of epigenetic mechanisms of plants and animals-theoretical considerations.Genetics & epigenetics · 2013Review
- H2A.Z acidic patch couples chromatin dynamics to regulation of gene expression programs during ESC differentiation.PLoS genetics · 2013Article
- Mutations in non-acid patch residues disrupt H2A.Z's association with chromatin through multiple mechanisms.PloS one · 2013Article
- Histone H2A variants in nucleosomes and chromatin: more or less stable?Nucleic acids research · 2012Review
- H2A.Z.2.2 is an alternatively spliced histone H2A.Z variant that causes severe nucleosome destabilization.Nucleic acids research · 2012Article
- A conserved function for the H2A.Z C terminus.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
The incorporation of histone variants into nucleosomes represents one way of altering the chromatin structure to accommodate diverse functions. Histone variant H2A.Z has specific roles in gene regulation, heterochromatin boundary formation, and genomic integrity. The precise features required for H2A.Z to function and specify an identity different from canonical H2A remain to be fully explored. Analysis of the C-terminal docking domain of H2A.Z in Saccharomyces cerevisiae using epistatic miniarray profile (E-MAP) uncovered nuanced requirements of the H2A.Z C-terminal region for cell growth when additional genes were compromised. Moreover, the H2A.Z(1-114) truncation, lacking the last 20 amino acids of the protein, did not support regular H2A.Z functions, such as resistance to genotoxic stress, restriction of heterochromatin in its native context, GAL1 gene activation, and chromatin anchoring. The corresponding region of H2A could fully rescue the strong defects caused by loss of this functionally essential region in the C terminus of H2A.Z. Despite the dramatic reduction in function, the H2A.Z(1-114) truncation still bound the H2A.Z deposition complex SWR1-C, the histone chaperone Chz1, and histone H2B. These data are consistent with a model in which retaining the variant in chromatin after its deposition by SWR1-C is a crucial determinant of its function.
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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.