Loss of H3.1K27me1 in Arabidopsis confers resistance to Geminivirus by sequestering DNA repair proteins onto host genome [ChIP-seq]

We identified RAD51 and RPA1A as partners of virus-encoded Rep protein. The two DNA repair proteins showed increased binding to heterochromatic regions and defense-related genes in atxr5 atxr6 vs wild-type plants. Consequently, the proteins had reduced binding to viral DNA in the mutant, thus hampering viral amplification. Additionally, RAD51 recruitment to the host genome arose via BRCA1, HOP2, and CYCB1;1, and this recruitment was essential for viral resistance in atxr5 atxr6. Thus, Geminiviruses adapt to healthy plants by hijacking DNA repairing pathways, whereas the unstable genome, triggered by lack of H3.1K27me1, could retain DNA repairing proteins to suppress viral infection in atxr5 atxr6. We first validated the specificity of anti-RAD51 and RPA1A antibodies (Extended Data Fig. 8. a-f), and then performed genome-wide chromatin immunoprecipitation-sequencing (ChIP-seq) for the two proteins in Col-0 and atxr5 atxr6.