The CmTGA1–CmRbohD Cascade Confers Resistance Against Chrysanthemum White Rust by Promoting Reactive Oxygen Species Generation

ABSTRACT Chrysanthemum white rust (CWR), caused by Puccinia horiana Heen., is a serious disease of chrysanthemum worldwide. This disease reduces the quality and yield of Chrysanthemum morifolium , leading to significant losses for chrysanthemum growers and industries. It is often referred to as the ‘cancer’ of chrysanthemum. The most effective approach to managing CWR is to utilise host resistance. Reactive oxygen species (ROS) are conserved basic defence compounds in higher plants that are generated in response to biotic stresses. This study reported the TGACG‐binding (TGA) transcription factor 1 ( CmTGA1 ) in chrysanthemum. Subcellular localisation analysis revealed that CmTGA1 is localised in the nucleus and cytoplasm. Overexpression or knockout of CmTGA1 in chrysanthemum increased or reduced CWR resistance by regulating ROS generation, the activities of antioxidant enzymes, and CmRbohD (a gene mediating ROS generation) expression. Yeast one‐hybrid, dual‐luciferase, and electrophoretic mobility shift assays showed that CmTGA1 bound directly to the as‐1 element in the promoter region of CmRbohD . Subcellular localisation analysis revealed that CmRbohD was localised in the cytomembrane and cytoplasm. CmRbohD was induced by P . horiana infection and enhanced CWR resistance by promoting ROS generation, activating the antioxidant enzyme system, and catalysing lignin biosynthesis. Our results showed that CmTGA1 activated CmRbohD to improve the CWR resistance via the ROS pathway in chrysanthemum. Our findings provided novel insights into the regulatory pathways involving the CmTGA1‐CmRbohD cascade‐mediated regulation of CWR resistance, demonstrating an effective strategy to improve tolerance to P . horiana in chrysanthemum.