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. Overall design: 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 ?-irradiation treatment of 40 Gy.