Many studies have focused on the plant hormone ethylene because of its key role in controlling, among others, climacteric fruit ripening and fruit senescence. These processes can be controlled by applying 1-MCP, which tightly binds to the ethylene receptors thereby blocking the ethylene signaling pathway. 1-MCP is known to inhibit the action of ethylene and to delay the climacteric ripening of tomato fruit. Less is known about its long term effect when the inhibitory effect 1-MCP inhibition is eventually released. Our objective was to study this transient 1-MCP inhibition during tomato fruit ripening in terms of fruit quality, ethylene production, respiration rate and the expression and protein abundance of receptors, CTRs and EIN2. For the identification and quantification of proteins, we used an LC–MS based targeted method of Parallel Reaction Monitoring (PRM), while gene expression was done using real time qPCR. Different color stages of tomatoes were harvested and treated with 1-MCP and subsequently stored to follow up postharvest fruit ripening. The difference with previous 1-MCP studies is that we sampled 1-MCP treated tomatoes at different physiological stages during ripening (and not time), matching the color stages of the untreated control fruit. This allows to properly compare the underlying regulation of the ethylene signaling pathway during a 1-MCP-mediated suppression of ripening. We hypothesized that the levels of the ethylene signaling components would be different for 1-MCP treated fruit due to a reduced ethylene-mediated autocatalytic feed-back. Our results showed that fruit treated with 1-MCP at mature green stage showed a lower respiration rate during subsequent ripening as compared to the untreated fruit, suggesting that climacteric ripening was effectively inhibited by 1-MCP. However, these 1-MCP treated fruit showed a higher ethylene production as compared to untreated fruit. The 1-MCP treated fruit also showed lower to equal levels of gene expression and protein abundance of the ethylene receptors, CTRs and EIN2. As receptors and CTRs are negative regulators of ethylene signaling, decreasing the production of new signaling proteins could subsequently activate downstream ethylene signaling and with that expression of downstream genes. This could lead to higher ethylene production levels, which in turn can compensate 1-MCP mediated inhibition of fruit ripening.

由于植物激素乙烯在控制更年期果实成熟和果实衰老等方面的关键作用，因此许多研究都集中在植物激素乙烯上。这些过程可以通过应用1-MCP来控制，该1-MCP与乙烯受体紧密结合，从而阻断了乙烯信号传导途径。已知1-MCP可抑制乙烯的作用并延迟番茄果实的更年期成熟。当1-MCP抑制作用最终被释放时，人们对其长期作用的了解还很少。我们的目的是研究番茄果实成熟过程中对1-MCP的短暂抑制，包括果实品质，乙烯产量，呼吸频率以及受体，CTR和EIN2的表达及蛋白丰度。为了鉴定和定量蛋白质，我们使用基于LC-MS的平行反应监测（PRM）的靶向方法，而基因表达则使用实时qPCR进行。收获番茄的不同颜色阶段，并用1-MCP处理，然后储存以跟踪收获后的果实成熟。与以前的1-MCP研究不同的是，我们在成熟过程中（而非时间上）在不同生理阶段对1-MCP处理过的西红柿进行了采样，匹配了未处理对照水果的颜色阶段。这允许在1-MCP介导的成熟抑制过程中正确比较乙烯信号传导途径的潜在调控。我们假设1-MCP处理的水果中乙烯信号成分的水平会有所不同，这是因为乙烯介导的自催化反馈减少。我们的结果表明，与未处理的水果相比，在未成熟的水果中用1-MCP处理的水果在随后的成熟过程中显示出较低的呼吸速率，这表明1-MCP可有效抑制更年期的成熟。然而，与未经处理的水果相比，这些经过1-MCP处理的水果显示出更高的乙烯产量。用1-MCP处理的果实还显示出较低的乙烯受体，CTR和EIN2的基因表达水平和蛋白质丰度。由于受体和CTR是乙烯信号的负调节剂，减少新信号蛋白的产生可随后激活下游乙烯信号并激活下游基因的表达。这可能导致更高的乙烯生产水平，进而可以补偿1-MCP介导的水果成熟抑制作用。