Abstract：
The gray mold fungus Botrytis cinerea is a necrotrophic pathogen that causes diseases in hundreds of plant species, including high-value crops. Its polyxenous nature and pathogenic success are due to its ability to perceive host signals in its favor. In this study, we found that laticifer cells of Euphorbia lathyris are a source of susceptibility factors required by B. cinerea to cause disease. Consequently, poor-in-latex (pil) mutants, which lack laticifer cells, show full resistance to this pathogen, whereas lot-of-latex mutants, which produce more laticifer cells, are hypersusceptible. These S factors are triterpenoid saponins, which are widely distributed natural products of vast structural diversity. The downregulation of laticifer-specific oxydosqualene cyclase genes, which encode the first committed step enzymes for triterpene and, therefore, saponin biosynthesis, conferred disease resistance to B. cinerea. Likewise, the Medicago truncatula lha-1 mutant, compromised in triterpenoid saponin biosynthesis, showed enhanced resistance. Interestingly, the application of different purified triterpenoid saponins pharmacologically complemented the disease-resistant phenotype of pil and hla-1 mutants and enhanced disease susceptibility in different plant species. We found that triterpenoid saponins function as plant cues that signal transcriptional reprogramming in B. cinerea, leading to a change in its growth habit and infection strategy, culminating in the abundant formation of infection cushions, the multicellular appressoria apparatus dedicated to plant penetration and biomass destruction in B. cinerea. Taken together, these results provide an explanation for how plant triterpenoid saponins function as disease susceptibility factors to promote B. cinerea pathogenicity.
摘要：
灰霉病菌灰霉病菌是一种坏死性病原体，在数百种植物中引起疾病，包括高价值作物。这种多异种性质和致病性成功归因于其感知宿主信号的能力。我们发现一品红的laticifer细胞是灰霉病产生疾病所需的易感性（S）因子的来源。因此,乳胶（pil）突变体，缺乏乳胶细胞，对这种病原体表现出完全的抗性，而乳胶（lol）突变体，产生更多的纤维细胞，是高度易感的。这些S因子是三萜皂苷，它们是广泛分布的结构多样性的天然产物。胶乳特异性羟角鲨烯环化酶（OSC）基因的下调，它编码三萜的第一步酶，因此,皂苷生物合成，赋予了对B.cinerea的抗病性。同样，Medicagotruncatulalha-1突变体,三萜皂苷生物合成受损，显示出增强的抗性。有趣的是,不同纯化的三萜皂苷的应用在药理学上补充了pil和hla-1突变体的抗病表型，并增强了不同植物物种的疾病易感性。我们发现三萜皂苷作为植物线索，在灰霉病中发出转录重编程的信号，导致其生长习惯和感染策略的改变，最终形成了丰富的感染垫(IC)，用于植物渗透和生物质破坏的多细胞无菌丝装置。我们的结果为植物三萜皂苷如何充当疾病易感性（S）因子以促进灰霉病的致病性提供了解释。
