RAD51 family factors remodel the NHEJ system to modulate stress-induced biosynthesis of diterpenoid phytoalexins in rice.

Double-strand break (DSB) damage are primarily repaired via homologous recombination (HR) and non-homologous end joining (NHEJ) in Eukaryotes. We reveals that HR subcomplex RAD51A1-RAD51C in rice (Oryza sativa L.) inhibits classic NHEJ pathway while acts as a transcriptional mediator underlying alternative NHEJ signaling. RAD51C hijacks the KU70 at DSBs, facilitated by its partner RAD51A1 or TOP6B responding environmental cues (pathogens and 4℃). Consequently, the enhanced alternative NHEJ signaling generates the phosphorylated SOG1, which activates the regulatory network in diterpenoid phytoalexin biosynthesis and a group of enzyme genes in phenylpropanoid pathway. Intriguingly, SOG1-BRCA1-RAD51 associates with RAD51C-RAD51D-XRCC3 to form a transcription pre-initiation complex in this process. Phenotypically, chemical disease resistance and 4℃-conditioned stomatal closure are compromised in single mutants (atm-3, sog1, and rad51c-1), double mutants (rad51a1 rad51a2 and rad51d xrcc3). In summary, HR pathway integrates classic and alternative NHEJ pathways to orchestrate stress-activated specific metabolism in rice. Hierarchical collaboration of global DSB-repair machinerys enable plant adaptability to DSB-related environmental stresses. RNA-seq assay in the leaves of sog1 mutant, rad51c xrcc3 double mutant and their WT ZH11 under normal condition or at 20 h after γ-irradiation treatment of 40 Gy.