Abstract Induced disease resistance of fruit by bio-based compounds is a promising strategy to control fruit decay. This research was aimed at studying the resistance of cherry tomato fruit to Botrytis cinerea induced by the yeast cell wall component from Saccharomyces cerevisiae and investigate a role of MAPKs in regulating the resistance response. The disease resistance of cherry tomato fruit was effectively enhanced by yeast cell wall and β-glucan. The expression of SlMAPK3 (but not of SlMAPK1 and SlMAPK2) was significantly increased by yeast cell wall and β-glucan and reached peak at 1 h. The yeast cell wall component also induced high expression of PR genes (SlPR1, SlPR5 and SlCHI9) and the transcription factors (SlERF1 and SlPti5) that specifically bind to the promoter of PR genes. The expression of PR genes (SlPR1, SlPR5 and SlCHI9) peaked after 24 h (at 24 or 48 h). The peak of SlERF1 and SlPti5 gene expression mostly appeared at around 4 h. It supposed to be a chronological order in the peaks of gene expression profile among SlMAPK3, PR genes and transcription factors. U0126 (1,4-diamino-2,3-dicyano-1,4-bis(o-amino-phenylmercapto)butadiene) significantly inhibited transcription of SlMAPK3, PR genes and transcription factors. The yeast cell wall and β-glucan could not induce high expression of SlMAPK3 and the downstream genes of SlMAPK3 in the U0126 treatment. These findings indicated that the yeast cell wall component that acts as microbe associated molecular patterns (MAMPs) could effectively induce disease resistance in cherry tomato fruit after harvest. The mechanism of induced resistance was associated with the expression of SlMAPK3 and defense-related genes. SlMAPK3, as an important upstream signaling kinase, had a direct regulatory effect on the downstream transcriptional factors (SlERF1 and SlPti5) to activate the expression of PR genes in the yeast cell wall component-induced immune responses in cherry tomato fruit.

中文翻译：

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SlMAPK3 是一种关键的丝裂原活化蛋白激酶，调节樱桃番茄果实对酵母细胞壁和 β-葡聚糖诱导的灰葡萄孢菌的抗性

摘要 通过生物基化合物诱导水果抗病性是控制水果腐烂的一种有前景的策略。本研究旨在研究由酿酒酵母的酵母细胞壁成分诱导的樱桃番茄果实对灰葡萄孢菌的抗性，并研究 MAPKs 在调节抗性反应中的作用。酵母细胞壁和β-葡聚糖有效增强了樱桃番茄果实的抗病性。酵母细胞壁和 β-葡聚糖显着增加了 SlMAPK3（但不是 SlMAPK1 和 SlMAPK2）的表达，并在 1 小时达到峰值。酵母细胞壁成分还诱导 PR 基因（SlPR1、SlPR5 和 SlCHI9）和与 PR 基因启动子特异性结合的转录因子（SlERF1 和 SlPti5）的高表达。PR基因（SlPR1，SlPR5 和 SlCHI9) 在 24 小时后（在 24 或 48 小时）达到峰值。SlERF1 和 SlPti5 基因表达的高峰主要出现在 4 h 左右。它应该是 SlMAPK3、PR 基因和转录因子之间基因表达谱峰值的时间顺序。U0126 (1,4-diamino-2,3-dicyano-1,4-bis(o-amino-phenylmercapto)butadiene) 显着抑制 SlMAPK3、PR 基因和转录因子的转录。U0126处理中酵母细胞壁和β-葡聚糖不能诱导SlMAPK3和SlMAPK3下游基因的高表达。这些发现表明，作为微生物相关分子模式 (MAMP) 的酵母细胞壁成分可以有效地诱导收获后樱桃番茄果实的抗病性。诱导抗性的机制与SlMAPK3和防御相关基因的表达有关。SlMAPK3 作为重要的上游信号激酶，对下游转录因子（SlERF1 和 SlPti5）具有直接调节作用，以激活樱桃番茄果实酵母细胞壁成分诱导免疫反应中 PR 基因的表达。