Kiwifruit are climacteric fruit, so they must be harvested before they are fully ripe, allowing for the extension of their shelf-life via cold storage. Therefore, an adequate knowledge about how ethylene-induced fruit senescence is required to avoid significant economic losses. The main goal of the present study was to investigate the kiwifruit ripening process at the physiological and molecular levels by RNA-seq after 1-methylcyclopropene (1-MCP, ethylene inhibitor) and Ethrel® (ethylene stimulator) treatments. The results showed that Ethrel® (ethephon) treatment induced more accelerated fruit ripening, leading to rapid fruit senescence, meanwhile 1-MCP caused a slowing flesh softening, and thus a longer shelf-life period. The RNA-seq was carried out on the fruit after 4 and 13 days, considering day 4 as the most determinant in terms of differentially expressed genes (DEGs). The sequencing achieved 70.7% alignment with the ‘Hongyang’ genome, obtaining 18,036 DEGs. The protein-protein interaction (PPI) network shows the interaction between different pathways in two main clusters: (1) pentose and glucoronate interconversions, citrate cycle, glycolysis and gluconeogenesis or starch, and sucrose metabolism and (2) porphyrin and chlorophyll metabolism. The first cluster is mainly interconnected by G6PD1 (pentose pathway); E1 ALPHA and ACLB-2 (citrate cycle); Achn209711 (pentose and glucoronate); LOS2 (glycolysis); HKL1 and HXK1 (glycolysis—starch and sucrose); and PHS2 (starch and sucrose). In the second cluster, GUN5 through PORA is interacting with CRD1 and NYC1 which were overexpressed by 1-MCP in the porphyrin and chlorophyll metabolism. In addition, genes linked to PSBY and PSBP photosynthesis-linked proteins in photosystem 2 were overexpressed by 1-MCP which is undoubtedly related to chlorophyll degradation and fruit senescence. These results suggest that in kiwifruit, the main pathways that are regulated by ethylene-induced senescence comprise sugar catabolism and chlorophyll degradation.

奇异果是更年期的水果，因此必须在完全成熟之前进行收获，以便通过冷藏来延长其保质期。因此，需要足够的知识来了解如何避免乙烯引起的果实衰老，从而避免重大的经济损失。本研究的主要目的是在1-甲基环丙烯（1-MCP，乙烯抑制剂）和Ethrel®（乙烯刺激剂）处理后，通过RNA-seq研究猕猴桃在生理和分子水平上的成熟过程。结果表明，Ethrel®（乙烯利）处理可加速果实成熟，导致果实快速衰老，同时1-MCP可使果肉变软，从而延长了货架期。在4天和13天后对水果进行RNA测序，考虑到第4天是差异表达基因（DEG）的最决定因素。测序结果与“弘扬”基因组比对达到70.7％，获得18,036个DEG。蛋白质-蛋白质相互作用（PPI）网络显示了两个主要簇中不同途径之间的相互作用：（1）戊糖和葡糖醛酸酯相互转化，柠檬酸循环，糖酵解和糖异生或淀粉以及蔗糖代谢和（2）卟啉和叶绿素代谢。第一个簇主要通过G6PD1（戊糖途径）相互连接。E1 ALPHA和ACLB-2（柠檬酸盐循环）；Achn209711（戊糖和葡萄糖酸）; LOS2（糖酵解）；HKL1和HXK1（糖酵解淀粉和蔗糖）；和PHS2（淀粉和蔗糖）。在第二个集群中 通过PORA的GUN5与在卟啉和叶绿素代谢中被1-MCP过表达的CRD1和NYC1相互作用。另外，光系统2中与PSBY和PSBP光合作用相关蛋白相关的基因被1-MCP过表达，这无疑与叶绿素降解和果实衰老有关。这些结果表明，在猕猴桃中，受乙烯诱导的衰老调节的主要途径包括糖分解代谢和叶绿素降解。