ArticlePloS one2009
The SNF2-family member Fun30 promotes gene silencing in heterochromatic loci.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 84 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
- Deposition of CENP-ACse4 is enhanced by mutations in the AAA+ ATPase domain of ATAD2Yta7.Genetics · 2026Article
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- Sir2 and Fun30 regulate ribosomal DNA replication timing via MCM helicase positioning and nucleosome occupancy.bioRxiv : the preprint server for biology · 2024Article
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- Swi/Snf chromatin remodeling regulates transcriptional interference and gene repression.Molecular cell · 2024Article
- Meiotic DNA break resection and recombination rely on chromatin remodeler Fun30.bioRxiv : the preprint server for biology · 2024Article
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- A SAM-key domain required for enzymatic activity of the Fun30 nucleosome remodeler.Life science alliance · 2023Article
- Genome-Wide Identification and Characterization of Major RNAi Genes Highlighting Their Associated Factors in Cowpea (BioMed research international · 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
- The regulation of DNA end resection by chromatin response to DNA double strand breaks.Frontiers in cell and developmental biology · 2022Review
- Loss of smarcad1a accelerates tumorigenesis of malignant peripheral nerve sheath tumors in zebrafish.Genes, chromosomes & cancer · 2021Article
- SMARCAD1 is an ATP-dependent histone octamer exchange factor with de novo nucleosome assembly activity.Science advances · 2021Article
- R-Loops and Its Chro-Mates: The Strange Case of Dr. Jekyll and Mr. Hyde.International journal of molecular sciences · 2021Review
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chromatin regulates many key processes in the nucleus by controlling access to the underlying DNA. SNF2-like factors are ATP-driven enzymes that play key roles in the dynamics of chromatin by remodelling nucleosomes and other nucleoprotein complexes. Even simple eukaryotes such as yeast contain members of several subfamilies of SNF2-like factors. The FUN30/ETL1 subfamily of SNF2 remodellers is conserved from yeasts to humans, but is poorly characterized. We show that the deletion of FUN30 leads to sensitivity to the topoisomerase I poison camptothecin and to severe cell cycle progression defects when the Orc5 subunit is mutated. We demonstrate a role of FUN30 in promoting silencing in the heterochromatin-like mating type locus HMR, telomeres and the rDNA repeats. Chromatin immunoprecipitation experiments demonstrate that Fun30 binds at the boundary element of the silent HMR and within the silent HMR. Mapping of nucleosomes in vivo using micrococcal nuclease demonstrates that deletion of FUN30 leads to changes of the chromatin structure at the boundary element. A point mutation in the ATP-binding site abrogates the silencing function of Fun30 as well as its toxicity upon overexpression, indicating that the ATPase activity is essential for these roles of Fun30. We identify by amino acid sequence analysis a putative CUE motif as a feature of FUN30/ETL1 factors and show that this motif assists Fun30 activity. Our work suggests that Fun30 is directly involved in silencing by regulating the chromatin structure within or around silent loci.
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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.