Zhao Lanfei, Su Peisen, Hou Bingqian, Wu Hongyan, Fan Yanhui, Li Wen, Zhao Jinxiao, Ge Wenyang, Xu Shoushen, Wu Shiwen, Ma Xin, Li Anfei, Bai Guihua, Wang Hongwei, Kong Lingrang
State Key Laboratory of Crop Biology, Shandong Key Laboratory of Crop Biology, College of Agronomy, Shandong Agricultural University, Tai'an, China.
Department of Agronomy, Kansas State University, Manhattan, KS, United States.
Front Plant Sci. 2022 Jun 30;13:926621. doi: 10.3389/fpls.2022.926621. eCollection 2022.
Fusarium head blight, mainly incited by , is a devastating wheat disease worldwide. Diverse Fusarium head blight (FHB) resistant sources have been reported, but the resistance mechanisms of these sources remain to be investigated. FHB-resistant wheat germplasm often shows black necrotic lesions (BNLs) around the infection sites. To determine the relationship between BNL and FHB resistance, leaf tissue of a resistant wheat cultivar Sumai 3 was inoculated with four different isolates. Integrated metabolomic and transcriptomic analyses of the inoculated samples suggested that the phytohormone signaling, phenolamine, and flavonoid metabolic pathways played important roles in BNL formation that restricted extension. Exogenous application of flavonoid metabolites on wheat detached leaves revealed the possible contribution of flavonoids to BNL formation. Exogenous treatment of either salicylic acid (SA) or methyl jasmonate (MeJA) on wheat spikes significantly reduced the FHB severity. However, exogenous MeJA treatment prevented the BNL formation on the detached leaves of FHB-resistant wheat Sumai 3. SA signaling pathway influenced reactive oxygen species (ROS) burst to enhance BNL formation to reduce FHB severity. Three key genes in SA biosynthesis and signal transduction pathway, , , and , positively regulated FHB resistance in wheat. A complex temporal interaction that contributed to wheat FHB resistance was detected between the SA and JA signaling pathways. Knowledge of BNLs extends our understanding of the molecular mechanisms of FHB resistance in wheat and will benefit the genetic improvement of wheat FHB resistance.
赤霉病主要由[病原体名称缺失]引起，是一种在全球范围内具有毁灭性的小麦病害。已报道了多种抗赤霉病（FHB）的资源，但这些资源的抗性机制仍有待研究。抗FHB的小麦种质在感染部位周围常出现黑色坏死斑（BNLs）。为了确定BNLs与FHB抗性之间的关系，用四种不同的[病原体名称缺失]分离株接种了抗性小麦品种苏麦3的叶片组织。对接种样品的综合代谢组学和转录组学分析表明，植物激素信号传导、酚胺和类黄酮代谢途径在限制[病原体名称缺失]扩展的BNLs形成中起重要作用。在小麦离体叶片上外源施用类黄酮代谢物揭示了类黄酮对BNLs形成的可能贡献。在小麦穗上外源施用水杨酸（SA）或茉莉酸甲酯（MeJA）均显著降低了FHB的严重程度。然而，外源MeJA处理阻止了抗FHB小麦苏麦3离体叶片上BNLs的形成。SA信号通路影响活性氧（ROS）爆发，以增强BNLs形成，从而降低FHB严重程度。SA生物合成和信号转导途径中的三个关键基因[基因名称缺失]、[基因名称缺失]和[基因名称缺失]正向调节小麦对FHB的抗性。在SA和JA信号通路之间检测到一种复杂的时间相互作用，有助于小麦对FHB的抗性。对BNLs的了解扩展了我们对小麦FHB抗性分子机制的认识，并将有利于小麦FHB抗性的遗传改良。
