BrCNGC12 and BrCNGC16 mediate Ca2+ absorption and transport to enhance resistance to tipburn in Chinese cabbage

Abstract

SummaryTipburn is a common physiological disorder in leafy vegetables, significantly impairing crop growth and commercial value. It is widely recognized that Ca2+ deficiency is a key factor triggering tipburn; however, the functions and regulatory mechanisms of genes conferring resistance remain largely unexplored. Through transcriptomic analysis of Chinese cabbage under normal (medium calcium, MCa) and Ca2+‐deficient (low calcium, LCa) conditions, we observed that genes in the hormone and calcium signalling pathways exhibited significant responses to LCa stress. Among these, the cyclic nucleotide‐gated ion channel (CNGC) genes BrCNGC12 and BrCNGC16, part of the calcium signalling pathway, were notably up‐regulated and down‐regulated, respectively, under LCa stress. Silencing BrCNGC12 in Chinese cabbage improves Ca2+ absorption and distribution, which strengthens tipburn resistance. Conversely, under LCa stress, heterologous expression of BrCNGC16 in Arabidopsis thaliana increases resistance to tipburn, whereas partial silencing of BrCNGC16 in Chinese cabbage diminishes resistance, with both outcomes linked to altered Ca2+ uptake and translocation. Additionally, overexpression of BrCNGC16 in Chinese cabbage promotes Ca2+ uptake and translocation, thereby enhancing resistance to tipburn and mitigating oxidative damage induced by Ca2+ deficiency. In conclusion, BrCNGC12 and BrCNGC16 play pivotal roles in tipburn resistance in Chinese cabbage, offering novel insights into the interplay between the calcium signalling pathway and tipburn resistance.