ArticleNucleic acids research2013
Histone methyltransferase SETD2 coordinates FACT recruitment with nucleosome dynamics during transcription.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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113 citing papers in PubMed, 176 citations in OpenAlex.
- Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6.Nucleic acids research · 2026Article
- Cryptic transcription in aging.iScience · 2026Review
- Integrated transcriptomic analysis reveals KRAS-associated gene activation and epigenetic regulation in mutant IDH1 glioma.Genes & genomics · 2026Article
- A U1-U3 snRNA-snoRNA interaction couples SF3B1 mutation to chromatin-state rewiring and genome instability.bioRxiv : the preprint server for biology · 2026Article
- Precision Medicine Gene Network Analyser: part I-cancer driver gene identification through network topology and ensemble machine learning.Genomics & informatics · 2026Article
- Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6.bioRxiv : the preprint server for biology · 2026Article
- SETD2 methyltransferase activity promotes correct transcription initiation and termination.EMBO reports · 2026Article
- The SETD2 L1609P mutation found in leukemia disrupts methyltransferase activity and reduces histone H3K36 trimethylation.The Journal of biological chemistry · 2026Article
- Loss of SETD2-mediated H3K36me3 Drives CD8Research (Washington, D.C.) · 2026Article
- Characterizing the Clinical and Molecular Profile of SETD2-Mutated Lung Adenocarcinoma.Cancers · 2025Article
- Emerging role of SETD2 in the development and function of immune cells.Genes & diseases · 2025Review
- Transcript diversity in aging: cryptic transcription and splicing.Medical review (2021) · 2025Review
- A SETD2-CDK1-lamin axis maintains nuclear morphology and genome stability.Nature cell biology · 2025Article
- Beyond Chaperoning: The Multifaceted Role of FACT in Chromatin Transactions.International journal of molecular sciences · 2025Review
- SETD2 loss of function is a recurrent event in advanced-phase chronic myeloid leukemia and contributes to genomic instability: SETD2 loss in Chronic Myeloid Leukemia.Clinical and translational medicine · 2025Article
- Elevated reactive oxygen species can drive the alternative lengthening of telomeres pathway in ATRX-null cancers.Nucleic acids research · 2025Article
- SETD2 loss-of-function uniquely sensitizes cells to epigenetic targeting of NSD1-directed H3K36 methylation.Genome biology · 2025Article
- Histone Modification Pathways Suppressing Cryptic Transcription.Epigenomes · 2024Article
- Repression of pervasive antisense transcription is the primary role of fission yeast RNA polymerase II CTD serine 2 phosphorylation.Nucleic acids research · 2024Article
- The histone methyltransferase SETD2 regulates HIV expression and latency.PLoS pathogens · 2024Article
53 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone H3 of nucleosomes positioned on active genes is trimethylated at Lys36 (H3K36me3) by the SETD2 (also termed KMT3A/SET2 or HYPB) methyltransferase. Previous studies in yeast indicated that H3K36me3 prevents spurious intragenic transcription initiation through recruitment of a histone deacetylase complex, a mechanism that is not conserved in mammals. Here, we report that downregulation of SETD2 in human cells leads to intragenic transcription initiation in at least 11% of active genes. Reduction of SETD2 prevents normal loading of the FACT (FAcilitates Chromatin Transcription) complex subunits SPT16 and SSRP1, and decreases nucleosome occupancy in active genes. Moreover, co-immunoprecipitation experiments suggest that SPT16 is recruited to active chromatin templates, which contain H3K36me3-modified nucleosomes. Our results further show that within minutes after transcriptional activation, there is a SETD2-dependent reduction in gene body occupancy of histone H2B, but not of histone H3, suggesting that SETD2 coordinates FACT-mediated exchange of histone H2B during transcription-coupled nucleosome displacement. After inhibition of transcription, we observe a SETD2-dependent recruitment of FACT and increased histone H2B occupancy. These data suggest that SETD2 activity modulates FACT recruitment and nucleosome dynamics, thereby repressing cryptic transcription initiation.
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