Ca2+ deficiency disrupts ROS homeostasis and induces tip burn in Chinese cabbage

Abstract Ca 2+ deficiency causes irreversible physiological disorders that markedly reduce the yield and quality of many horticultural crops, leading to substantial economic losses. Tip burn in Chinese cabbage ( Brassica rapa ssp. pekinensis ) is associated with Ca 2+ deficiency; however, the underlying molecular mechanisms remain poorly understood. In this study, Ca 2+ deficiency suppressed growth and impaired photosynthetic performance in Chinese cabbage seedlings. Under Ca 2+ deficiency, cytosolic Ca 2+ levels decreased, accompanied by excessive reactive oxygen species (ROS) accumulation in the leaves. Foliar application of dimethylthiourea (DMTU), an ROS scavenger, alleviated Ca 2+ deficiency-induced tip burn by reducing ROS accumulation. RNA-seq analysis further revealed significant enrichment of the mitogen-activated protein kinase signaling and plant hormone signal transduction pathways during tip-burn development. Several differentially expressed genes associated with these pathways were identified as responsive to Ca 2+ deficiency. Compared with normal Ca 2+ and DMTU-rescued conditions, the respiratory burst oxidase homolog D ( BrRbohD-2 ) gene was markedly upregulated under Ca 2+ deficiency. Overexpression of BrRbohD-2 increased ROS accumulation and aggravated tip burn in Chinese cabbage seedlings, whereas its suppression reduced ROS levels and alleviated tip burn. These findings provide important insights into the role of BrRbohD-2 and the regulatory mechanisms underlying Ca 2+ deficiency-related disorders in Brassicaceae crops.