Premature Mesocarp Vitality Loss in Niagara Rosada Occurs Independently of Cell Death

The grape berry mesocarp experiences key physiological changes during ripening, often including mesocarp cell death (MCD). We hypothesized that MCD does not occur in the Niagara Rosada (NR) variety but rather a downregulation of respiratory enzymes during the early loss of mesocarp cell vitality, with membrane integrity preserved. Using label-free proteomics, enzymatic activity assays, and outer mesocarp imaging, we observed intact cytoplasmic membranes, alongside with reduced mitochondrial cristae density, malate dehydrogenase, and succinate dehydrogenase activities. Proteomic analysis revealed 956 differentially accumulated proteins, with most downregulated at ripening. However, several glycolytic enzymes remained abundant at ripening, suggesting maintenance of respiratory activity despite mesocarp physiological changes, such as stress-induced and senescence-related proteins that were upregulated at veraison. We further hypothesized that gluconeogenesis originated from malate operates in the mesocarp and that sucrose futile cycles may play a crucial role in carbohydrate storage and unloading. Therefore, we suggest that the premature loss of mesocarp vitality in NR is not linked to cell death but rather a senescence adaptation.