A Cotton Laccase Confers Disease Resistance Against Verticillium dahliae by Promoting Cell Wall Lignification.

IF 4.8 1区 农林科学 Q1 PLANT SCIENCES
Guanfu Cheng, Chuanzong Li, Guoshuai Zhang, W G Dilantha Fernando, Yanqing Bi, Jianfeng Lei, Peihong Dai, Xiaofeng Su, Yue Li
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Abstract

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.

一种棉花漆酶通过促进细胞壁木质化来抵抗大丽花黄萎病。
黄萎病(Verticillium wilt, VW)主要由大丽花黄萎病(Verticillium dahliae)引起,严重威胁棉花生产。植物细胞壁的木质化是一种由病原体入侵引发的防御反应,对植物抵抗许多疾病至关重要。漆酶参与次生细胞壁的木质化,但在棉花抗大丽花中的作用尚不完全清楚。在这项研究中,我们发现了一个棉花漆酶基因GhLAC14-3,该基因在早期大丽花v感染期间显著上调,并且与先前报道的拟南芥中对大丽花v感染作出反应的基因密切相关。在棉花中沉默GhLAC14-3增加了疾病易感性,减少了木质素沉积和木质素相关基因的表达。相比之下,转基因拟南芥中过表达GhLAC14-3增加了木质素含量和木质素相关基因的表达,从而增强了对VW的抗性。我们在细胞膜上发现了GhLAC14-3和丝裂原激活蛋白激酶GhMAPKKK2之间的相互作用。GhMAPKKK2在棉花中也被大丽花病菌感染显著诱导表达,其在拟南芥中的过表达激活了多个关键抗性基因,从而提高了大丽花病菌的抗性。GhMAPKKK2和GhLAC14-3在烟叶中的瞬时共表达显著提高了木质素含量。相反,在ghlac14 -3过表达的拟南芥中,沉默AtMAPKKK2 (GhMAPKKK2的同源物)会降低木质素水平和抗病性。我们的研究结果表明,GhLAC14-3是增强大众抗性的一个有希望的靶点,因为它与细胞膜上的GhMAPKKK2相互作用调节防御诱导的木质素化。
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来源期刊
Molecular plant pathology
Molecular plant pathology 生物-植物科学
CiteScore
9.40
自引率
4.10%
发文量
120
审稿时长
6-12 weeks
期刊介绍: Molecular Plant Pathology is now an open access journal. Authors pay an article processing charge to publish in the journal and all articles will be freely available to anyone. BSPP members will be granted a 20% discount on article charges. The Editorial focus and policy of the journal has not be changed and the editorial team will continue to apply the same rigorous standards of peer review and acceptance criteria.
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