ArticleNucleic acids research2019
A conserved genetic interaction between Spt6 and Set2 regulates H3K36 methylation.
Article in Nucleic acids research, 2019. 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, 50 citations in OpenAlex.
- Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6.Nucleic acids research · 2026Article
- Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6.bioRxiv : the preprint server for biology · 2026Article
- Structural basis of transcription-coupled H3K36 trimethylation by Set2 in coordination with FACT.Science advances · 2026Article
- Molecular mechanism of co-transcriptional H3K36 methylation by SETD2.Nature communications · 2025Article
- Overlapping and distinct functions of SPT6, PNUTS, and PCF11 in regulating transcription termination.Nucleic acids research · 2025Article
- Structural basis of H3K36 trimethylation by SETD2 during chromatin transcription.Science (New York, N.Y.) · 2025Article
- Multiple direct and indirect roles of the Paf1 complex in transcription elongation, splicing, and histone modifications.Cell reports · 2024Article
- Repression of pervasive antisense transcription is the primary role of fission yeast RNA polymerase II CTD serine 2 phosphorylation.Nucleic acids research · 2024Article
- Di- and tri-methylation of histone H3K36 play distinct roles in DNA double-strand break repair.Science China. Life sciences · 2024Article
- Multiple direct and indirect roles of Paf1C in elongation, splicing, and histone post-translational modifications.bioRxiv : the preprint server for biology · 2024Article
- Insights into Spt6: a histone chaperone that functions in transcription, DNA replication, and genome stability.Trends in genetics : TIG · 2023Review
- Cooperative assembly confers regulatory specificity and long-term genetic circuit stability.Cell · 2023Article
- Spt6 directly interacts with Cdc73 and is required for Paf1 complex occupancy at active genes in Saccharomyces cerevisiae.Nucleic acids research · 2023Article
- The conserved histone chaperone Spt6 is strongly required for DNA replication and genome stability.Cell reports · 2023Article
- Histone methyltransferase SETD2: An epigenetic driver in clear cell renal cell carcinoma.Frontiers in oncology · 2023Review
- Proteomic analysis reveals changes in the proteome of human THP-1 macrophages infected withFrontiers in cellular and infection microbiology · 2023Article
- The histone methyltransferase SETD2 negatively regulates cell size.Journal of cell science · 2022Article
- Suppressor mutations that make the essential transcription factor Spn1/Iws1 dispensable in Saccharomyces cerevisiae.Genetics · 2022Article
- Applying the auxin-based degron system for the inducible, reversible and complete protein degradation iniScience · 2022Article
- Cooperation between intrinsically disordered and ordered regions of Spt6 regulates nucleosome and Pol II CTD binding, and nucleosome assembly.Nucleic acids research · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription elongation factor Spt6 and the H3K36 methyltransferase Set2 are both required for H3K36 methylation and transcriptional fidelity in Saccharomyces cerevisiae. However, the nature of the requirement for Spt6 has remained elusive. By selecting for suppressors of a transcriptional defect in an spt6 mutant, we have isolated several highly clustered, dominant SET2 mutations (SET2sup mutations) in a region encoding a proposed autoinhibitory domain. SET2sup mutations suppress the H3K36 methylation defect in the spt6 mutant, as well as in other mutants that impair H3K36 methylation. We also show that SET2sup mutations overcome the requirement for certain Set2 domains for H3K36 methylation. In vivo, SET2sup mutants have elevated levels of H3K36 methylation and the purified Set2sup mutant protein has greater enzymatic activityin vitro. ChIP-seq studies demonstrate that the H3K36 methylation defect in the spt6 mutant, as well as its suppression by a SET2sup mutation, occurs at a step following the recruitment of Set2 to chromatin. Other experiments show that a similar genetic relationship between Spt6 and Set2 exists in Schizosaccharomyces pombe. Taken together, our results suggest a conserved mechanism by which the Set2 autoinhibitory domain requires multiple Set2 interactions to ensure that H3K36 methylation occurs specifically on actively transcribed chromatin.
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