ArticleNature communications2023
H3.1K27me1 loss confers Arabidopsis resistance to Geminivirus by sequestering DNA repair proteins onto host genome.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- A novel genetic framework reveals transcriptional "butterfly effect" underlying heterosis in maize.Journal of advanced research · 2026Article
- Chromatin remodeling by HIRA and FAS2 restricts geminivirus pathogenesis in plants.Virology journal · 2026Article
- T-DNAreader: fast and precise identification of T-DNA insertion sites in plant genomes using RNA sequencing data.Genome biology · 2025Article
- Evaluation of soybean germplasms for resistance to stay-green syndrome.Scientific reports · 2025Article
- A new scheme for boosting in situ Fenton-like reaction in plant pathogenic tissues for selective structural degradation of capsid proteins.Journal of nanobiotechnology · 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
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
The H3 methyltransferases ATXR5 and ATXR6 deposit H3.1K27me1 to heterochromatin to prevent genomic instability and transposon re-activation. Here, we report that atxr5 atxr6 mutants display robust resistance to Geminivirus. The viral resistance is correlated with activation of DNA repair pathways, but not with transposon re-activation or heterochromatin amplification. We identify RAD51 and RPA1A as partners of virus-encoded Rep protein. The two DNA repair proteins show increased binding to heterochromatic regions and defense-related genes in atxr5 atxr6 vs wild-type plants. Consequently, the proteins have reduced binding to viral DNA in the mutant, thus hampering viral amplification. Additionally, RAD51 recruitment to the host genome arise via BRCA1, HOP2, and CYCB1;1, and this recruitment is essential for viral resistance in atxr5 atxr6. Thus, Geminiviruses adapt to healthy plants by hijacking DNA repair pathways, whereas the unstable genome, triggered by reduced H3.1K27me1, could retain DNA repairing proteins to suppress viral amplification in atxr5 atxr6.
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