Cheng Guanfu, Li Chuanzong, Zhang Guoshuai, Fernando W G Dilantha, Bi Yanqing, Lei Jianfeng, Dai Peihong, Su Xiaofeng, Li Yue
Xinjiang Key Laboratory for Ecological Adaptation and Evolution of Extreme Environment Biology, College of Life Sciences, Xinjiang Agricultural University, Xinjiang, China.
National Key Laboratory of Agricultural Microbiology, Biotechnology Research Institute, Chinese Academy of Agricultural Sciences, Beijing, China.
Mol Plant Pathol. 2025 Jul;26(7):e70125. doi: 10.1111/mpp.70125.
Verticillium wilt (VW), caused primarily by Verticillium dahliae, is a significant threat to cotton production. Lignification of the plant cell wall, a defence response triggered by pathogen invasion, is critical for plant resistance to numerous diseases. Laccases are known to participate in the lignification of secondary cell walls, but their role in cotton resistance to V. dahliae is not fully understood. In this study, we identified a cotton laccase gene, GhLAC14-3, that was significantly upregulated during early V. dahliae infection and was closely related to a gene previously reported to respond to V. dahliae infection in Arabidopsis. Silencing of GhLAC14-3 in cotton increased disease susceptibility and reduced lignin deposition and the expression of lignin-related genes. By contrast, overexpression of GhLAC14-3 in transgenic Arabidopsis increased lignin content and the expression of lignin-related genes, thereby enhancing VW resistance. We identified an interaction between GhLAC14-3 and the mitogen-activated protein kinase GhMAPKKK2 at the cell membrane. GhMAPKKK2 expression was also significantly induced by V. dahliae infection in cotton, and its overexpression in Arabidopsis activated multiple key resistance genes, thus improving V. dahliae resistance. Transient co-expression of GhMAPKKK2 and GhLAC14-3 in Nicotiana benthamiana leaves significantly increased lignin content. Conversely, silencing of AtMAPKKK2, the homologue of GhMAPKKK2, in GhLAC14-3-overexpressing Arabidopsis reduced both lignin levels and disease resistance. Our findings suggest that GhLAC14-3 is a promising target for enhancing VW resistance, as its interaction with GhMAPKKK2 at the cell membrane modulates defence-induced lignification.
黄萎病主要由大丽轮枝菌引起，对棉花生产构成重大威胁。植物细胞壁木质化是病原体入侵引发的一种防御反应，对植物抵抗多种病害至关重要。已知漆酶参与次生细胞壁的木质化过程，但其在棉花抵抗大丽轮枝菌中的作用尚未完全明确。在本研究中，我们鉴定出一个棉花漆酶基因GhLAC14 - 3，该基因在大丽轮枝菌早期感染期间显著上调，且与先前报道的拟南芥中响应大丽轮枝菌感染的一个基因密切相关。在棉花中沉默GhLAC14 - 基因增加了病害易感性，减少了木质素沉积以及木质素相关基因的表达。相比之下，在转基因拟南芥中过表达GhLAC14 - 3增加了木质素含量以及木质素相关基因的表达，从而增强了对黄萎病的抗性。我们确定了GhLAC14 - 3与丝裂原活化蛋白激酶GhMAPKKK2在细胞膜上存在相互作用。棉花中GhMAPKKK2的表达也在大丽轮枝菌感染后被显著诱导，其在拟南芥中的过表达激活了多个关键抗性基因，从而提高了对大丽轮枝菌的抗性。在本氏烟草叶片中瞬时共表达GhMAPKKK2和GhLAC14 - 3显著增加了木质素含量。相反，在过表达GhLAC14 - 3的拟南芥中沉默GhMAPKKK2的同源基因AtMAPKKK2，降低了木质素水平和抗病性。我们的研究结果表明，GhLAC14 - 3是增强黄萎病抗性的一个有前景的靶点，因为它与GhMAPKKK2在细胞膜上的相互作用调节了防御诱导的木质化过程。
