ArticleThe Journal of biological chemistry2013
The ATP-dependent chromatin remodeling enzyme Fun30 represses transcription by sliding promoter-proximal nucleosomes.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Slx4 and Fun30/SMARCAD1 coordinate S-phase checkpoint regulation and replication fork protection in response to Top1-DNA crosslinks.Nucleic acids research · 2026Article
- A pangenome of maize provides genetic insights into drought resistance.Nature genetics · 2025Article
- Meiotic DNA break resection and recombination rely on chromatin remodeler Fun30.bioRxiv : the preprint server for biology · 2024Article
- Article
- A SAM-key domain required for enzymatic activity of the Fun30 nucleosome remodeler.Life science alliance · 2023Article
- Fun30 and Rtt109 Mediate Epigenetic Regulation of the DNA Damage Response Pathway inJournal of fungi (Basel, Switzerland) · 2022Article
- Arabidopsis CHROMATIN REMODELING 19 acts as a transcriptional repressor and contributes to plant pathogen resistance.The Plant cell · 2022Article
- R-Loops and Its Chro-Mates: The Strange Case of Dr. Jekyll and Mr. Hyde.International journal of molecular sciences · 2021Review
- SMARCAD1-mediated active replication fork stability maintains genome integrity.Science advances · 2021Article
- An embryonic stem cell-specific heterochromatin state promotes core histone exchange in the absence of DNA accessibility.Nature communications · 2020Article
- Role of the ATP-dependent chromatin remodeling enzyme Fun30/Smarcad1 in the regulation of mRNA splicing.Biochemical and biophysical research communications · 2020Article
- Smarcad1 mediates microbiota-induced inflammation in mouse and coordinates gene expression in the intestinal epithelium.Genome biology · 2020Article
- The Mechanism of Chromatin Remodeler SMARCAD1/Fun30 in Response to DNA Damage.Frontiers in cell and developmental biology · 2020Review
- SMARCAD1 ATPase activity is required to silence endogenous retroviruses in embryonic stem cells.Nature communications · 2019Article
- Nucleosome Remodeling by Fun30Frontiers in molecular biosciences · 2019Review
- Yeast Systems Biology: The Continuing Challenge of Eukaryotic Complexity.Methods in molecular biology (Clifton, N.J.) · 2019Article
- The CUE1 domain of the SNF2-like chromatin remodeler SMARCAD1 mediates its association with KRAB-associated protein 1 (KAP1) and KAP1 target genes.The Journal of biological chemistry · 2018Article
- It's fun to transcribe with Fun30: A model for nucleosome dynamics during RNA polymerase II-mediated elongation.Transcription · 2018Article
- DNA repair goes hip-hop: SMARCA and CHD chromatin remodellers join the break dance.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- SNF2 Family Protein Fft3 Suppresses Nucleosome Turnover to Promote Epigenetic Inheritance and Proper Replication.Molecular cell · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The evolutionarily conserved ATP-dependent chromatin remodeling enzyme Fun30 has recently been shown to play important roles in heterochromatin silencing and DNA repair. However, how Fun30 remodels nucleosomes is not clear. Here we report a nucleosome sliding activity of Fun30 and its role in transcriptional repression. We observed that Fun30 repressed the expression of genes involved in amino acid and carbohydrate metabolism, the stress response, and meiosis. In addition, Fun30 was localized at the 5' and 3' ends of genes and within the open reading frames of its targets. Consistent with its role in gene repression, we observed that Fun30 target genes lacked histone modifications often associated with gene activation and showed an increased level of ubiquitinated histone H2B. Furthermore, a genome-wide nucleosome mapping analysis revealed that the length of the nucleosome-free region at the 5' end of a subset of genes was changed in Fun30-depleted cells. In addition, the positions of the -1, +2, and +3 nucleosomes at the 5' end of target genes were shifted significantly, whereas the position of the +1 nucleosome remained largely unchanged in the fun30Δ mutant. Finally, we demonstrated that affinity-purified, single-component Fun30 exhibited a nucleosome sliding activity in an ATP-dependent manner. These results define a role for Fun30 in the regulation of transcription and indicate that Fun30 remodels chromatin at the 5' end of genes by sliding promoter-proximal nucleosomes.
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Registered trials
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.