Levels of ethylene, implicated in a diverse array of plants for inducing fruit ripening, is influenced by genetic and environmental factors, such as the other plant hormones. Among these, salicylic acid (SA) and its derivative, acetylsalicylic acid (ASA) have been demonstrated to inhibit ethylene biosynthesis in fruit, yet the underlying regulatory mechanisms remains elusive. Here, we showed that treatment with exogenous ASA dramatically reduced ethylene production, as well as activities of ACC synthase (ACS) and ACC oxidase (ACO), in kiwifruit tissues. Comparative transcriptome analysis indicated the differential expression of ethylene biosynthetic genes (AdACS1/2 and AdACO5). A screen of transcription factors indicated that AdERF105L and AdWRKY29 were ASA-responsive regulators of AdACS1/2 and AdACO5, respectively. In addition to these genes, AdACS3 and AdACO3 were abundantly expressed in both ASA-treated and control tissues. AdACS3 protein was phosphorylated and stabilized by AdMPK16, a mitogen-activated protein kinase; while AdACO3 activity was enhanced by AdAP, an aspartic peptidase. Exogenous ASA down-regulated AdMPK16 and AdAP, thereby influencing ethylene biosynthesis at a post-transcriptional level. These findings propose a multidimensional system for ASA-inhibition on ethylene biosynthesis, inducing differential expression of some ethylene biosynthesis genes, as well as differential effects on protein activity on other targets.

中文翻译：

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猕猴桃外源乙酰水杨酸对乙烯生物合成的转录和转录后调控

乙烯水平与多种植物诱导果实成熟有关，受遗传和环境因素（如其他植物激素）的影响。其中，水杨酸 (SA) 及其衍生物乙酰水杨酸 (ASA) 已被证明可抑制水果中乙烯的生物合成，但其潜在的调节机制仍然难以捉摸。在这里，我们发现外源性 ASA 处理显着降低了猕猴桃组织中乙烯的产生以及 ACC 合酶 (ACS) 和 ACC 氧化酶 (ACO) 的活性。比较转录组分析表明乙烯生物合成基因（AdACS1/2和AdACO5）的差异表达。转录因子筛选表明 AdERF105L 和 AdWRKY29 分别是 AdACS1/2 和 AdACO5 的 ASA 响应调节因子。除了这些基因，AdACS3 和 AdACO3 在 ASA 处理和对照组织中均大量表达。AdACS3 蛋白被有丝分裂原活化蛋白激酶 AdMPK16 磷酸化和稳定；而天冬氨酸肽酶 AdAP 增强了 AdACO3 的活性。外源性 ASA 下调 AdMPK16 和 AdAP，从而影响转录后水平的乙烯生物合成。这些发现提出了一个多维系统，用于 ASA 对乙烯生物合成的抑制，诱导一些乙烯生物合成基因的差异表达，以及对其他靶点的蛋白质活性的不同影响。外源性 ASA 下调 AdMPK16 和 AdAP，从而影响转录后水平的乙烯生物合成。这些发现提出了一个多维系统，用于 ASA 对乙烯生物合成的抑制，诱导一些乙烯生物合成基因的差异表达，以及对其他靶点的蛋白质活性的不同影响。外源性 ASA 下调 AdMPK16 和 AdAP，从而影响转录后水平的乙烯生物合成。这些发现提出了一个多维系统，用于 ASA 对乙烯生物合成的抑制，诱导一些乙烯生物合成基因的差异表达，以及对其他靶点的蛋白质活性的不同影响。