Abstract Continuous ethylene supplementation suppresses postharvest sprouting, but it can increase reducing sugars, limiting its use as an alternative to chlorpropham for processing potatoes. To elucidate the mechanisms involved, tubers were treated after curing with or without the ethylene binding inhibitor 1-methylcyclopropene (1-MCP at 1 μL L−1 for 24 h), and then stored in air or air supplemented with continuous ethylene (10 μL L−1). Across three consecutive seasons, changes in tuber physiology were assessed alongside transcriptomic and metabolomic analysis. Exogenous ethylene alone consistently induced a respiratory rise and the accumulation of undesirable reducing sugars. The transient respiratory peak was preceded by the strong upregulation of two genes encoding 1-aminocyclopropane-1-carboxylate oxidase (ACO), typical of wound and stress induced ethylene production. Profiles of parenchymatic tissue highlighted that ethylene triggered abscisic acid (ABA) catabolism, evidenced by a steep fall in ABA levels and a transient rise in the catabolite phaseic acid, accompanied by upregulation of transcripts encoding an ABA 8ˊ-hydroxylase. Moreover, analysis of non-structural carbohydrate-related genes revealed that ethylene strongly downregulated the expression of the Kunitz-type invertase inhibitor, already known to be involved in cold-induced sweetening. All these ethylene-induced effects were negated by 1-MCP with one notable exception: 1-MCP enhanced the sprout suppressing effect of ethylene whilst preventing ethylene-induced sweetening. This study supports the conclusions that: i) tubers adapt to ethylene by regulating conserved pathways (e.g. ABA catabolism); ii) ethylene-induced sweetening acts independently from sprout suppression, and is similar to cold-induced sugar accumulation.

中文翻译：

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乙烯对贮藏马铃薯块茎中 ABA 分解代谢、增甜和休眠影响的新见解

摘要 连续补充乙烯会抑制收获后的发芽，但它会增加还原糖，限制了其作为氯苯丙胺加工马铃薯的替代品的使用。为了阐明所涉及的机制，在使用或不使用乙烯结合抑制剂 1-甲基环丙烯（1-MCP 在 1 μL L-1 中 24 小时）固化后对块茎进行处理，然后储存在空气中或补充有连续乙烯（10 μL）的空气中。 L-1)。在连续三个季节中，与转录组学和代谢组学分析一起评估了块茎生理学的变化。外源性乙烯单独持续引起呼吸上升和不希望的还原糖的积累。短暂的呼吸峰值之前是两个编码 1-氨基环丙烷-1-羧酸氧化酶 (ACO) 的基因的强烈上调，典型的伤口和压力诱导乙烯产生。实质组织的特征突出显示，乙烯引发脱落酸 (ABA) 分解代谢，ABA 水平急剧下降，分解代谢产物相酸短暂上升，伴随着编码 ABA 8ˊ-羟化酶的转录本的上调，证明了这一点。此外，对非结构性碳水化合物相关基因的分析表明，乙烯强烈下调 Kunitz 型转化酶抑制剂的表达，已知该抑制剂与冷诱导的甜味有关。所有这些乙烯诱导的作用都被 1-MCP 抵消，但有一个显着的例外：1-MCP 增强了乙烯的发芽抑制作用，同时防止了乙烯诱导的甜味。该研究支持以下结论：i) 块茎通过调节保守途径（例如 ABA分解代谢）；ii) 乙烯诱导的增甜作用独立于萌芽抑制，类似于冷诱导的糖积累。