Abstract

Spongy tissue, as one of internal flesh breakdown in mango fruits, is correlated with calcium (Ca) deficiency, and adversely affects fruit quality and yield worldwide. However, the underlying mechanism causing spongy tissue remains unknown. Here, we explored the effects of Ca deficiency on spongy tissue in a susceptible cultivar, ‘Keitt’, at the physiological and molecular levels. Nutrient analysis showed that flesh with spongy tissue had lower Ca content and higher N/Ca, K/Ca and Mg/Ca rations than healthy fruit flesh. Ca accumulation in the cell wall, especially in chelator-soluble pectin, was elevated due to increased pectin content, lower levels of pectin methylesterification, and increased pectin methylesterase (PME) activity. During spongy tissue development, levels of Ca oxalate (CaOx) and oxalic acid both increased, whereas soluble Ca content decreased in the flesh. Transcriptomic analysis of healthy flesh and flesh with spongy tissue revealed 2054 up-regulated and 996 down-regulated genes. Gene ontology term analysis showed that the up-regulated genes were mainly enriched in functions related to the transmembrane transporter activity, calcium ion binding, and the cell wall. Importantly, up-regulated genes in spongy tissue included five glucuronate 4-epimerase (GAE) genes and two galactosyltransferase (GALT) genes, which involved in pectin synthesis; four PME genes which control pectin demethylesterification; and eight autoinhibited calcium-transporting ATPase (ACA) genes and two vacuole H+/Ca2+ exchanger (CAX) genes which contribute to Ca influx in the vacuole. Our findings illustrate a mechanism by which Ca deficiency leads to spongy tissue, which will contribute to efforts to control this physiological disorder.

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