Botrytis cinerea, the causal agent of the grey mould disease, developed resistance to multiple fungicides. However, the role of cell membrane in survival competition of B. cinerea upon quinone outside inhibitor (QoI) fungicide has not yet been elucidated. In this paper, the enhancement of cystamine, a transglutaminase inhibitor, on membrane integrity of B. cinerea was determined, and the effect of the enhancement on the sensitivity of B. cinerea to pyraclostrobin was investigated. The results showed that pyraclostrobin inhibited mycelial growth with EC₅₀ as 1.122 and 3.042 μg/ml at 24 and 48 hr, respectively. In the treatment of 5 and 50 μg/ml pyraclostrobin, membrane integrity of B. cinerea was broken, causing high permeability, lipid peroxidation, flocculent and malformed surface with vague septum and abundant agglomerates inside and outside the mycelia. Cystamine even at 50 and 200 μg/ml had little inhibitory effect on mycelial growth. However, in presence of 50 or 200 μg/ml cystamine, the mycelia from pyraclostrobin treatment possessed a significantly reduced leakage, lower MDA content, and a revived fibrous and transparent surface. Meanwhile, SEM images showed that membrane integrity of the mycelia was significantly improved and the agglomerates were dramatically disappeared. Synergy assays further revealed that B. cinerea regained less sensitivity to pyraclostrobin inhibition. In conclusion, membrane integrity controls mycelia sensitivity and is required for survival competition of B. cinerea upon pyraclostrobin.

中文翻译：

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膜完整性对灰葡萄孢对 QoI 杀菌剂唑菌胺酯生存竞争的影响

Botrytis cinerea 是灰霉病的病原体，对多种杀菌剂产生抗药性。然而，细胞膜在 B. cinerea 对醌外抑制剂 (QoI) 杀菌剂的生存竞争中的作用尚未阐明。在本文中，确定了胱胺（一种转谷氨酰胺酶抑制剂）对 B. cinerea 膜完整性的增强作用，并研究了增强作用对 B. cinerea 对唑菌胺酯敏感性的影响。结果表明，唑菌胺酯在 24 和 48 小时抑制菌丝体生长，EC 50 分别为 1.122 和 3.042 μg/ml。在 5 和 50 μg/ml 唑菌胺酯处理中，B. cinerea 的膜完整性被破坏，导致高渗透性、脂质过氧化、表面呈絮状、畸形，间隔模糊，菌丝内外有丰富的团聚体。即使在 50 和 200 μg/ml 的胱胺对菌丝体生长也几乎没有抑制作用。然而，在存在 50 或 200 μg/ml 胱胺的情况下，唑菌胺酯处理的菌丝体具有显着减少的泄漏、较低的 MDA 含量和恢复的纤维状透明表面。同时，SEM图像显示菌丝体的膜完整性显着提高，团聚体显着消失。协同分析进一步揭示了灰霉病菌对唑菌胺酯抑制的敏感性降低。总之，膜完整性控制菌丝体敏感性，并且是灰霉病菌对唑菌胺酯的生存竞争所必需的。即使在 50 和 200 μg/ml 的胱胺对菌丝体生长也几乎没有抑制作用。然而，在存在 50 或 200 μg/ml 胱胺的情况下，唑菌胺酯处理的菌丝体具有显着减少的泄漏、较低的 MDA 含量和恢复的纤维状透明表面。同时，SEM图像显示菌丝体的膜完整性显着提高，团聚体显着消失。协同分析进一步揭示了灰霉病菌对唑菌胺酯抑制的敏感性降低。总之，膜完整性控制菌丝体敏感性，并且是灰霉病菌对唑菌胺酯的生存竞争所必需的。即使在 50 和 200 μg/ml 的胱胺对菌丝体生长也几乎没有抑制作用。然而，在存在 50 或 200 μg/ml 胱胺的情况下，唑菌胺酯处理的菌丝体具有显着减少的泄漏、较低的 MDA 含量和恢复的纤维状透明表面。同时，SEM图像显示菌丝体的膜完整性显着提高，团聚体显着消失。协同分析进一步揭示了灰霉病菌对唑菌胺酯抑制的敏感性降低。总之，膜完整性控制菌丝体敏感性，并且是灰霉病菌对唑菌胺酯的生存竞争所必需的。和恢复的纤维和透明的表面。同时，SEM图像显示菌丝体的膜完整性显着提高，团聚体显着消失。协同分析进一步揭示了灰霉病菌对唑菌胺酯抑制的敏感性降低。总之，膜完整性控制菌丝体敏感性，并且是灰霉病菌对唑菌胺酯的生存竞争所必需的。和恢复的纤维和透明的表面。同时，SEM图像显示菌丝体的膜完整性显着提高，团聚体显着消失。协同分析进一步揭示了灰霉病菌对唑菌胺酯抑制的敏感性降低。总之，膜完整性控制菌丝体敏感性，并且是灰霉病菌对唑菌胺酯的生存竞争所必需的。