Chen Xiao-Hua, Li Xiao-Min, Deng Jie, Li Jin-Mei, Liu Di-Qiu
Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, Yunnan, China.
Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, Yunnan, China.
Int J Biol Macromol. 2025 May;307(Pt 3):142249. doi: 10.1016/j.ijbiomac.2025.142249. Epub 2025 Mar 18.
Fusarium wilt is a significant problem restricting the growth of the lily industry. However, Lilium regale Wilson is a valuable germplasm resource because of its Fusarium Wilt resistance. In this study, six endo-β-1,4-glucanase genes (Cel1-Cel6) in L. regale were identified among the differentially expressed genes reveled by omics data for L. regale infected Fusarium osysporum, which causes Fusarium wilt. Interestingly, the abundance of a few proteins and the expression of endo-β-1,4-glucanase genes, including LrCel1, decreased in L. regale roots infected with F. oxysporum. Thus, the function of LrCel1 in the incompatible interaction between L. regale and F. oxysporum was analyzed. LrCel1 expression was inhibited by F. oxysporum and salicylic acid (SA). Additionally, the subcellular localization of LrCel1 revealed it was a cell membrane protein. The ectopic expression of LrCel1 increased of susceptibility of tobacco to F. oxysporum because of the associated increase in cellulase activity, which, hindered the production of cellulose, callose, and lignin. Moreover, LrCel1 overexpression inhibited the accumulation of SA and jasmonic acid (JA), resulting in the down-regulated expression of genes associated with SA/JA signaling pathways. Conversely, introducing an RNAi vector targeting LrCel1 into L. regale enhanced the resistance to F. oxysporum, likely because of an increase in the synthesis of cellulose, callose, and lignin as well as a decrease in the expression of JA/SA signaling pathway genes. In addition, LrCel1 promoter activity was suppressed by F. oxysporum and Fusarium solani as well as SA. Furthermore, a positive regulator of Fusarium wilt resistance, LrWRKY11, negatively regulated LrCel1 promoter activity. The study findings have elucidated the intricate regulatory network of WRKY transcription factor and SA/JA signaling pathways to inhibit the cellulase activity of endo-β-1,4-glucanase in L. regale, thereby conferring resistance to Fusarium wilt.
枯萎病是限制百合产业发展的一个重大问题。然而,岷江百合因其对枯萎病具有抗性,是一种宝贵的种质资源。在本研究中,从感染尖孢镰刀菌(引起枯萎病)的岷江百合组学数据所揭示的差异表达基因中,鉴定出了岷江百合中的6个内切-β-1,4-葡聚糖酶基因(Cel1-Cel6)。有趣的是,在感染尖孢镰刀菌的岷江百合根系中,包括LrCel1在内的一些蛋白质丰度和内切-β-1,4-葡聚糖酶基因的表达下降。因此,分析了LrCel1在岷江百合与尖孢镰刀菌不亲和互作中的功能。LrCel1的表达受到尖孢镰刀菌和水杨酸(SA)的抑制。此外,LrCel1的亚细胞定位显示它是一种细胞膜蛋白。LrCel1的异位表达由于纤维素酶活性的相关增加而提高了烟草对尖孢镰刀菌的敏感性,这阻碍了纤维素、胼胝质和木质素的产生。此外,LrCel1的过表达抑制了SA和茉莉酸(JA)的积累,导致与SA/JA信号通路相关基因的表达下调。相反,将靶向LrCel1的RNAi载体导入岷江百合增强了对尖孢镰刀菌的抗性,这可能是由于纤维素、胼胝质和木质素的合成增加以及JA/SA信号通路基因的表达降低。此外,LrCel1启动子活性受到尖孢镰刀菌、茄病镰刀菌以及SA的抑制。此外,枯萎病抗性的正向调节因子LrWRKY11对LrCel1启动子活性起负向调节作用。研究结果阐明了WRKY转录因子与SA/JA信号通路抑制岷江百合内切-β-1,4-葡聚糖酶纤维素酶活性的复杂调控网络,从而赋予对枯萎病的抗性。