ArticleGenes & development2011
Structural basis for the role of the Sir3 AAA+ domain in silencing: interaction with Sir4 and unmethylated histone H3K79.
Article in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Molecular and regulatory aspects of EPA: a Nakaseomyces glabratus epithelial adhesin.Archives of microbiology · 2026Review
- Physical interactions within the SIR heterochromatin complex potentiate inter-subunit communication and gene repression.Cell reports · 2026Article
- Transcriptional silencing in Saccharomyces cerevisiae: known unknowns.Epigenetics & chromatin · 2024Review
- Review
- Histone H2B ubiquitylation: Connections to transcription and effects on chromatin structure.Biochimica et biophysica acta. Gene regulatory mechanisms · 2024Review
- Article
- Sir3 heterochromatin protein promotes non-homologous end joining by direct inhibition of Sae2.The EMBO journal · 2022Article
- Measuring the buffering capacity of gene silencing inProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Conserved crosstalk between histone deacetylation and H3K79 methylation generates DOT1L-dose dependency in HDAC1-deficient thymic lymphoma.The EMBO journal · 2019Article
- Proteomic profiling of yeast heterochromatin connects direct physical and genetic interactions.Current genetics · 2019Article
- The interplay of histone H2B ubiquitination with budding and fission yeast heterochromatin.Current genetics · 2018Review
- Yeast heterochromatin regulators Sir2 and Sir3 act directly at euchromatic DNA replication origins.PLoS genetics · 2018Article
- Recruitment and allosteric stimulation of a histone-deubiquitinating enzyme during heterochromatin assembly.The Journal of biological chemistry · 2018Article
- Article
- A D53 repression motif induces oligomerization of TOPLESS corepressors and promotes assembly of a corepressor-nucleosome complex.Science advances · 2017Article
- Variants of the Sir4 Coiled-Coil Domain Improve Binding to Sir3 for Heterochromatin Formation inG3 (Bethesda, Md.) · 2017Article
- Article
- The upstreams and downstreams of H3K79 methylation by DOT1L.Chromosoma · 2016Review
- The Nuts and Bolts of Transcriptionally Silent Chromatin in Saccharomyces cerevisiae.Genetics · 2016Review
- Cooperative stabilization of the SIR complex provides robust epigenetic memory in a model of SIR silencing in Saccharomyces cerevisiae.Epigenetics · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The silent information regulator 2/3/4 (Sir2/3/4) complex is required for gene silencing at the silent mating-type loci and at telomeres in Saccharomyces cerevisiae. Sir3 is closely related to the origin recognition complex 1 subunit and consists of an N-terminal bromo-adjacent homology (BAH) domain and a C-terminal AAA(+) ATPase-like domain. Here, through a combination of structure biology and exhaustive mutagenesis, we identified unusual, silencing-specific features of the AAA(+) domain of Sir3. Structural analysis of the putative nucleotide-binding pocket in this domain reveals a shallow groove that would preclude nucleotide binding. Mutation of this site has little effect on Sir3 function in vivo. In contrast, several surface regions are shown to be necessary for the Sir3 silencing function. Interestingly, the Sir3 AAA(+) domain is shown here to bind chromatin in vitro in a manner sensitive to histone H3K79 methylation. Moreover, an exposed loop on the surface of this Sir3 domain is found to interact with Sir4. In summary, the unique folding of this conserved Sir3 AAA(+) domain generates novel surface regions that mediate Sir3-Sir4 and Sir3-nucleosome interactions, both being required for the proper assembly of heterochromatin in living cells.
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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.