Jiao Wenli, Lei Tianyi, Duan Qingyu, Wang Jingyuan, Yang Yushan, Li Guang, Zhang Rongbao, Pan Hongyu, Zhang Yanhua
College of Plant Sciences, Jilin University, Changchun, China.
Baicheng Academy of Agricultural Sciences, Baicheng, China.
Mol Plant Pathol. 2025 Apr;26(4):e70088. doi: 10.1111/mpp.70088.
Microorganisms use versatile strategies to facilitate the colonisation of hosts, through remodelling transcription and metabolism to accommodate growth under harsh and hostile environments. Sclerotinia sclerotiorum is a typical necrotrophic pathogen that causes Sclerotinia stem rot in more than 700 species, resulting in serious economic losses. How S. sclerotiorum integrates mechanisms for nutrient acquisition and utilisation to maintain optimal growth and pathogenicity is still indistinct. Here, we demonstrate that Ndt80 family transcription factors (SsNdt80a,b,c) are involved in carbon source utilisation and have different roles in the growth, sclerotia formation, infection cushion development, and the virulence of S. sclerotiorum. SsNdt80b could bind the promoter of SsSNF1 and modulate the transcriptional activity of SsSNF1. Silencing SsSNF1 resulted in defects in hyphal growth and infection cushion formation, reduced cell wall-degrading enzymes, and reduced pathogenicity of S. sclerotiorum. A model is proposed in which SsNdt80b responds to carbon sources and modulates SsSnf1 to regulate the development and pathogenicity of S. sclerotiorum.
微生物通过重塑转录和代谢以适应在恶劣和不利环境下的生长,利用多种策略促进对宿主的定殖。核盘菌是一种典型的坏死营养型病原菌,可在700多种植物上引起菌核病,造成严重经济损失。核盘菌如何整合营养获取和利用机制以维持最佳生长和致病性仍不清楚。在此,我们证明Ndt80家族转录因子(SsNdt80a、b、c)参与碳源利用,并在核盘菌的生长、菌核形成、侵染垫发育和致病性中发挥不同作用。SsNdt80b可结合SsSNF1的启动子并调节SsSNF1的转录活性。沉默SsSNF1会导致菌丝生长和侵染垫形成缺陷、细胞壁降解酶减少以及核盘菌致病性降低。我们提出了一个模型,其中SsNdt80b响应碳源并调节SsSnf1以调控核盘菌的发育和致病性。