Silicon-induced tissue-specific reprogramming of the ripening transition in kiwifruit

Silicon is recognized for its protective role under (a)biotic stress, yet its influence on fruit ripening remains largely unexplored. Here, ‘Hayward’ kiwifruit was used as a model to investigate the effects of external Si application on placenta and pericarp ripening. Silicon predominantly accumulated in placenta and pedicel junction, resulting in delayed ripening. This delay was associated with altered ethylene signaling, particularly via modulation of AP2/ERF transcription factors, and modifications in cell wall structure, including increased arabinogalactan proteins and altered homogalacturonan methyl-esterification. Also, silicon induced tissue-specific metabolic shifts, notably in sugars, organic acids, and polyphenolic biosynthesis, including the anthocyanin–proanthocyanidin branch point. Extensive transcriptomic reprogramming following silicon application, especially in placenta, highlighted its key role in early silicon responses. Proteins such as lipoxygenase, 60S ribosomal protein L28 and carboxypeptidases were commonly regulated in both pericarp and placenta during late cold storage, suggesting roles in ripening initiation. Proteogenomic integration identified conserved elements, like 1-aminocyclopropane-1-carboxylate oxidase, and highlighted post-transcriptional regulation under cold storage. Comparison with calcium-treatment data revealed partially overlapping silicon–calcium responses, including ethylene suppression and structural remodeling. These findings establish silicon as a novel regulator of kiwifruit ripening and provide a valuable resource for exploring its role in kiwifruit and other fruits.