RAD51-Mediated DNA Repair and its Emerging Role in Plant–Virus Interactions: A Comprehensive Review
Abstract
Maintenance of genome integrity is indispensable for plant growth, reproduction, and adaptation to environmental stress. Homologous recombination (HR) is a high-fidelity pathway for the repair of DNA double-strand breaks, and the ATP-dependent recombinase RAD51 is its central catalytic component. RAD51 forms a nucleoprotein filament on resected single-stranded DNA, conducts homology search, and promotes strand invasion, while BRCA2, RPA, RAD54, and RAD51 paralogs regulate filament assembly and downstream processing. An emerging body of evidence shows that this repair machinery also participates in interactions between plants and nuclear-replicating DNA viruses, particularly geminiviruses. Because geminiviruses do not encode a complete DNA replication apparatus, they redirect host cell-cycle, replication, recombination, and chromatin factors to convert viral single-stranded DNA into double-stranded intermediates and to amplify viral minichromosomes through rolling-circle and recombination-dependent replication. Experimental studies have implicated RAD54, RAD51D, RAD51, RPA1A, DNA primase, and DNA polymerases á and ä in these processes. Conversely, plants can restrict infection by transcriptional immune mechanisms and by altering the genomic distribution of repair proteins. In Arabidopsis, BRCA2–RAD51 and SNI1–RAD51D modules connect salicylic-acid-responsive defense-gene transcription with recombination, whereas loss of H3.1K27me1 redistributes RAD51 and RPA1A from viral DNA to unstable host chromatin and defense-associated loci, reducing geminiviral amplification. Recent identification of resistance-associated alleles in host DNA primase and DNA polymerase ä further establishes replication proteins as practical targets for crop improvement. This review integrates canonical RAD51 biology with current evidence from plant–geminivirus systems, distinguishes established mechanisms from model-dependent observations, and outlines research priorities for exploiting host repair and replication pathways without compromising genome stability.