Objectives To determine the effect of sea salt on the resistance of Trichoderma harzianum LZDX-32-08 to hygromycin B and speculate the possible mechanisms involved via transcriptome analysis. Results Sea salt addition in media to simulate marine environment significantly increased the tolerance of marine-derived fungus Trichoderma harzianum LZDX-32-08 to hygromycin B from 40 to 500 μg/ml. Meanwhile, sea salt addition also elicited the hygromycin B resistance of 5 other marine or terrestrial fungi. Transcriptomic analyses of T. harzianum cultivated on PDA, PDA supplemented with sea salt and PDA with both sea salt and hygromycin B revealed that genes coding for P-type ATPases, multidrug resistance related transporters and acetyltransferases were up-regulated, while genes coding for Ca 2+ /H + antiporter and 1,3-glucosidase were down-regulated, indicating probable increased efflux and inactivation of hygromycin B as well as enhanced biofilm formation, which could jointly contribute to the drug resistance. Conclusions Marine environment or high ion concentration in the environment could be an importance inducer for antifungal resistance. Possible mechanisms and related key genes were proposed for understanding the molecular basis and overcoming this resistance.

中文翻译：

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海盐诱导哈茨木霉LZDX-32-08对潮霉素B的抗性增强

目的 确定海盐对哈茨木霉 LZDX-32-08 对潮霉素 B 抗性的影响，并通过转录组分析推测可能的机制。结果在培养基中添加海盐以模拟海洋环境显着增加了海洋来源的真菌哈茨木霉 LZDX-32-08 对潮霉素 B 的耐受性，从 40 到 500 μg/ml。同时，海盐的添加也引发了其他 5 种海洋或陆生真菌对潮霉素 B 的抗性。在PDA、补充海盐的PDA和同时含有海盐和潮霉素B的PDA上培养的哈茨木霉的转录组学分析显示，编码P型ATP酶、多药耐药相关转运蛋白和乙酰转移酶的基因上调，而编码Ca的基因2+ /H + 逆向转运蛋白和 1,3-葡萄糖苷酶下调，表明可能增加潮霉素 B 的外排和失活以及增强的生物膜形成，这可能共同导致耐药性。结论海洋环境或环境中的高离子浓度可能是抗真菌抗性的重要诱导剂。为理解分子基础和克服这种抗性提出了可能的机制和相关的关键基因。