Elucidating the Molecular Mechanisms of Physiological Fruit Abscission in Actinidia arguta Through Comparative Transcriptomics and Transient Genetic Transformation

<i>Actinidia arguta</i> (<i>A. arguta</i>) is valued for its nutritional richness, but physiological fruit abscission severely limits production efficiency in elite cultivars. To unravel the molecular basis of this process, we compared two cultivars: abscission-prone 'KL' and abscission-resistant 'JL'. During fruit development, 'KL' exhibited an earlier decline in auxin (AUX) levels within the fruit abscission zone (FAZ), coupled with persistently higher ethylene (ETH) concentrations and polygalacturonase (PG) activity compared to 'JL'. Comparative transcriptomics identified abscission-related genes enriched in plant hormone signaling (AUX, ETH, ABA, JA, BR), starch/sucrose metabolism, and photosynthesis pathways. AUX signaling diverged predominantly during early development, while ETH, BR, and JA pathways varied across multiple stages. Exogenous applications of plant growth regulators (ethephon, 2,4-D, methyl jasmonate, and 2,4-epibrassinolide) and transient overexpression of key genes (<i>AaETR1</i>, <i>AaERF035</i>, <i>AaPME68</i>, <i>AaPP2C27</i>, <i>AaMYC1</i>, and <i>AaPMEI10</i>) validated their roles in modulating hormone crosstalk and cell wall remodeling. Overexpression of <i>AaERF035</i> and <i>AaPME68</i> likely accelerated abscission by enhancing ETH biosynthesis and pectin degradation, while <i>AaPMEI10</i> and <i>AaMYC1</i> potentially delayed abscission via suppression of cell wall-modifying enzymes. This study elucidates the hormonal and transcriptional networks governing fruit abscission in <i>A. arguta</i>, providing insights for targeted breeding and cultivation strategies to mitigate yield loss.