Maize ZmDLR2/BRU1 Is Required for Lateral Root Primordium Emergence by Participating in DNA Repair.

Lateral roots (LRs), the primary component of the maize root system, are crucial for water and nutrient acquisition. Deciphering the molecular mechanisms underlying LR formation and development is therefore essential for improving maize yield and stress resilience. In this study, we characterised a mutant, defective in lateral root 2-1 (dlr2-1), which displays impaired LR development and compromised drought resistance. Phenotypic analysis and RNA-seq revealed defective cell proliferation in lateral root primordia (LRP) of dlr2-1, likely attributable to DNA damage. Accordingly, the dlr2-1 mutant exhibited an activated DNA damage response. Exogenous treatment of wild-type B73 plants with genotoxic agents recapitulated the dlr2-1 phenotype, suppressing LRP emergence and reducing mature LR numbers. Positional cloning and allelic analysis pinpointed a missense mutation in DLR2, causing a leucine-to-glutamine substitution at residue 1035 (ZmDLR2^L1035Q) and accounting for the LR defects in dlr2-1. ZmDLR2 encodes a maize orthologue of Arabidopsis BRUSHY1 (BRU1), a key regulator of DNA damage repair during DNA replication. Comet assays demonstrated that dlr2-1 accumulates more severe DNA fragmentation than B73, as evidenced by an elevated tail moment, which was further aggravated under genotoxic stress. Moreover, ZmDLR2 mutation adversely affected plant height and kernel size in dlr2 mutants, leading to significant yield reduction. Collectively, our results establish that ZmDLR2 is indispensable for DNA repair and that its dysfunction activates the DNA damage response, ultimately inhibiting cell proliferation, disrupting LRP initiation and LR formation and compromising maize productivity.