ArticlePLoS genetics2016
Identification of Multiple Proteins Coupling Transcriptional Gene Silencing to Genome Stability in Arabidopsis thaliana.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Mutations in Components of the TREX-2 Complex Result in Misexpression of the Kelch-Domain F-Box Protein KFB39 Promoter inPlant direct · 2026Article
- Domestication shaped the chromatin landscape of grain amaranth.Nature communications · 2025Article
- Diurnal control of H3K27me1 deposition shapes expression of a subset of cell cycle and DNA damage response genes.The Plant journal : for cell and molecular biology · 2024Article
- Identification of plants' functional counterpart of the metazoan mediator of DNA Damage checkpoint 1.EMBO reports · 2024Article
- H3.1K27me1 loss confers Arabidopsis resistance to Geminivirus by sequestering DNA repair proteins onto host genome.Nature communications · 2023Article
- Article
- Distinct roles of Arabidopsis ORC1 proteins in DNA replication and heterochromatic H3K27me1 deposition.Nature communications · 2023Article
- The Role of the TSK/TONSL-H3.1 Pathway in Maintaining Genome Stability in Multicellular Eukaryotes.International journal of molecular sciences · 2022Review
- A Journey to the Core of the Plant Cell Cycle.International journal of molecular sciences · 2022Review
- Cycling in a crowd: Coordination of plant cell division, growth, and cell fate.The Plant cell · 2022Review
- The role of ATXR6 expression in modulating genome stability and transposable element repression inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- H3.1K27me1 maintains transcriptional silencing and genome stability by preventing GCN5-mediated histone acetylation.The Plant cell · 2021Article
- The making and unmaking of the silenced chromatin.The Plant cell · 2021Article
- Comparison of Metabolic Profiling ofPhenomics (Cham, Switzerland) · 2021Article
- DNA polymerase epsilon is required for heterochromatin maintenance in Arabidopsis.Genome biology · 2020Article
- Crosstalk between Ubiquitination and Other Post-translational Protein Modifications in Plant Immunity.Plant communications · 2020Review
- Nuclear pore complex-mediated gene expression in Arabidopsis thaliana.Journal of plant research · 2020Article
- A plant-specific SWR1 chromatin-remodeling complex couples histone H2A.Z deposition with nucleosome sliding.The EMBO journal · 2020Article
- Methyl-CpG-binding domain 9 (MBD9) is required for H2A.Z incorporation into chromatin at a subset of H2A.Z-enriched regions in the Arabidopsis genome.PLoS genetics · 2019Article
- Regulation of centromeric heterochromatin in the cell cycle by phosphorylation of histone H3 tyrosine 41.Current genetics · 2019Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Eukaryotic genomes are regulated by epigenetic marks that act to modulate transcriptional control as well as to regulate DNA replication and repair. In Arabidopsis thaliana, mutation of the ATXR5 and ATXR6 histone methyltransferases causes reduction in histone H3 lysine 27 monomethylation, transcriptional upregulation of transposons, and a genome instability defect in which there is an accumulation of excess DNA corresponding to pericentromeric heterochromatin. We designed a forward genetic screen to identify suppressors of the atxr5/6 phenotype that uncovered loss-of-function mutations in two components of the TREX-2 complex (AtTHP1, AtSAC3B), a SUMO-interacting E3 ubiquitin ligase (AtSTUbL2) and a methyl-binding domain protein (AtMBD9). Additionally, using a reverse genetic approach, we show that a mutation in a plant homolog of the tumor suppressor gene BRCA1 enhances the atxr5/6 phenotype. Through characterization of these mutations, our results suggest models for the production atxr5 atxr6-induced extra DNA involving conflicts between the replicative and transcriptional processes in the cell, and suggest that the atxr5 atxr6 transcriptional defects may be the cause of the genome instability defects in the mutants. These findings highlight the critical intersection of transcriptional silencing and DNA replication in the maintenance of genome stability of heterochromatin.
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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 Socratic graph.