Abstract Nitric Oxide (NO) is one of the most studied signalling molecules as it is an important modulator that interact with other molecules during plant defence mechanism against pathogen attack. The predominant regulatory mode of action of NO is protein S-nitrosylation - the covalent binding of NO moiety to the sulfhydryl group of cysteine residue to form S-nitrosothiol (SNO). In this study, we examined the potential role of NO in modulating the interaction of banana- Fusarium oxysporum f. sp. cubense Tropical Race 4. We demonstrated that pre-treatment of banana seedlings with NO donor S-nitrosoglutathione (GSNO) managed to delay Fusarium wilt symptom development, corresponding to a low disease severity index (DSI) whereas pre-treatment with NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) increased the DSI. GSNO treatment increased the SNO level from 57.6 μM mgˉ1 during the early stage of infection to 97 μM mgˉ1 in Foc TR4-challenged banana roots. Biotin switch assay also showed that the banana proteins are S-nitrosylated following inoculation with FocTR4. The findings of this study suggested that NO can improve the tolerance of banana to Foc TR4 through S-nitrosylation, as a molecular mechanism underlying the interaction between the FocTR4 and banana.

中文翻译：

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一氧化氮提高对尖孢镰刀菌 f 的耐受性。sp. 香蕉中的cubense Tropical Race 4

摘要 一氧化氮（NO）是研究最多的信号分子之一，因为它是一种重要的调节剂，在植物防御病原体攻击的防御机制中与其他分子相互作用。NO 的主要调节作用模式是蛋白质 S-亚硝基化 - NO 部分与半胱氨酸残基的巯基共价结合以形成 S-亚硝基硫醇 (SNO)。在这项研究中，我们研究了 NO 在调节香蕉-尖孢镰刀菌相互作用中的潜在作用。sp. cubense Tropical Race 4. 我们证明了用 NO 供体 S-亚硝基谷胱甘肽 (GSNO) 预处理香蕉幼苗成功延缓了枯萎病症状的发展，对应于低疾病严重度指数 (DSI)，而用 NO 清除剂预处理 2- phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) 增加了 DSI。在 Foc TR4 攻击的香蕉根中，GSNO 处理使 SNO 水平从感染早期的 57.6 μM mgˉ1 增加到 97 μM mgˉ1。生物素转换分析还表明，香蕉蛋白在接种 FocTR4 后发生 S-亚硝基化。这项研究的结果表明，NO 可以通过 S-亚硝基化提高香蕉对 Foc TR4 的耐受性，这是 FocTR4 与香蕉相互作用的分子机制。