Weed Research Laboratory, Nanjing Agricultural University, Nanjing 210095, China.
Department of Plant Physiology, Institute of Biology, Warsaw University of Life Sciences SGGW, 159 Nowoursynowska 159, 02-776 Warsaw, Poland.
Cells. 2021 Apr 25;10(5):1010. doi: 10.3390/cells10051010.
The necrotrophic fungus contains different pathotypes that produce different mycotoxins. The pathotype secretes the non-host-selective toxin tenuazonic acid (TeA), which can cause necrosis in many plants. Although TeA is thought to be a central virulence factor of the pathotype, the precise role of TeA in different stages of host infection by pathogens remains unclear. Here, an wild-type and the toxin-deficient mutant with a 75% reduction in TeA production were used. It was observed that wild-type pathogens could induce the reactive oxygen species (ROS) bursts in host leaves and killed photosynthetic cells before invading hyphae. The ROS interceptor catalase remarkably inhibited hyphal penetration and invasive hyphal growth and expansion in infected leaves and suppressed necrotic leaf lesion. This suggests that the production of ROS is critical for pathogen invasion and proliferation and disease symptom formation during infection. It was found that the mutant pathogens did not cause the formation of ROS and cell death in host leaves, showing an almost complete loss of disease susceptibility. In addition, the lack of TeA resulted in a significant reduction in the ability of the pathogen to penetrate invasive hyphal growth and spread. The addition of exogenous TeA, AAL-toxin, and bentazone to the mutant pathogens during inoculation resulted in a significant restoration of pathogenicity by increasing the level of cell death, frequency of hyphal penetration, and extent of invasive hyphal spread. Our results suggest that cell death triggered by TeA is the essential requirement for successful colonization and disease development in host leaves during infection with pathogens.
坏死型真菌包含不同的致病型，它们产生不同的真菌毒素。致病型 分泌非寄主选择性毒素 tenuazonic 酸（TeA），它可以导致许多植物坏死。尽管 TeA 被认为是 致病型的一个中心毒力因子，但 TeA 在病原体感染宿主的不同阶段的确切作用仍不清楚。在这里，使用了野生型和毒素缺陷突变体 ，其 TeA 产量减少了 75%。观察到野生型病原体可以在宿主叶片中诱导活性氧（ROS）爆发，并在侵入菌丝之前杀死光合细胞。ROS 拦截器过氧化氢酶显著抑制了感染叶片中菌丝的穿透和侵入性菌丝的生长和扩展，并抑制了坏死叶片损伤。这表明 ROS 的产生对于病原体的入侵和增殖以及感染过程中疾病症状的形成至关重要。研究发现，突变体病原体不会在宿主叶片中引起 ROS 的形成和细胞死亡，表现出几乎完全丧失对疾病的敏感性。此外，缺乏 TeA 导致病原体穿透和侵入性菌丝生长和传播的能力显著降低。在接种过程中向突变体 病原体中添加外源 TeA、AAL 毒素和苯达松，通过增加细胞死亡水平、菌丝穿透频率和侵入性菌丝扩散程度，显著恢复了致病性。我们的研究结果表明，在 病原体感染宿主叶片过程中，由 TeA 引发的细胞死亡是成功定殖和疾病发展的必要条件。
