4.5 Article

VdTps2 Modulates Plant Colonization and Symptom Development in Verticillium dahliae

期刊

MOLECULAR PLANT-MICROBE INTERACTIONS
卷 36, 期 9, 页码 572-583

出版社

AMER PHYTOPATHOLOGICAL SOC
DOI: 10.1094/MPMI-03-23-0024-R

关键词

melanized microsclerotia; penetration peg; ROS stress; Verticillium dahliae; virulence

向作者/读者索取更多资源

The trehalose biosynthesis pathway is important for the fungal pathogen Verticillium dahliae, with VdTps2 playing a critical role in hyphal growth, microsclerotia formation, stress resistance, and disease development.
The trehalose biosynthesis pathway is a potential target for antifungal drugs development. Trehalose phosphate synthase (TPS) and phosphatase are widely conserved components of trehalose biosynthesis in fungi. However, the role of trehalose biosynthesis in the vascular plant-pathogenic fungus Verticillium dahliae remains unclear. Here, we investigated the functions of the TPS complex, including VdTps1, VdTps2, and VdTps3 in V. dahliae. Unlike VdTps2, deletion of VdTps1 or VdTps3 did not alter any phenotypes compared with the wild-type strain. In contrast, the Delta VdTps2 strain showed severely depressed radial growth due to the abnormal swelling of the hyphal tips. Further, deletion of VdTps2 increased microsclerotia formation, melanin biosynthesis, and resistance to cell-wall perturbation and high-temperature stress. Virulence assays and quantification of fungal biomass revealed that deletion of VdTps2 delayed disease symptom development, as evident by the reduced virulence and decreased biomass of the Delta VdTps2 strain in plant stem tissue following inoculation. Additionally, increases in penetration peg formation observed in the Delta VdTps2 strain in the presence of H2O2 suggested that VdTps2 suppresses initial colonization. Our results also revealed the role of VdTps2 as a regulator of autophagy. Together, these results indicate that VdTps2 contributes to plant colonization and disease development.Copyright (c) 2023 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据