Abstract
As the corn aphid (Rhopalosiphum maidis) poses a major threat to maize (Zea mays) growth, there is much interest in identifying aphid resistance genes. In this study, an aphid-susceptible maize mutant from an ethyl methanesulfonate-mutagenized library is identified that exhibits greater aphid settlement than the wild type. Using the MutMap approach, the causal gene RESISTANCE TO APHIDS 9 (RTA9) is cloned, which encodes a mitochondrion-localized protein from the Domain of Unknown Function 641 family. Overexpressing RTA9 in maize confers significant resistance to aphids without compromising seed yield. It further identifies the senescence regulator S40 as an interactor of RTA9, which negatively regulates the stability of S40. Knockout of S40 enhanced aphid resistance, while its overexpression increased susceptibility. Further analysis demonstrates that the rta9-1 mutant does not exhibit significant enrichment of differentially expressed genes associated with oxidoreductase activity following aphid infestation. By contrast, genes involved in this pathway are significantly enriched in the s40 mutant. Additionally, aphid-induced reactive oxygen species (ROS) levels are markedly lower in rta9-1 than in the wild type but significantly higher in s40. Collectively, the results suggest that the mitochondrial protein RTA9 and its interacting partner S40 regulate resistance to aphid infestation by modulating ROS homeostasis.