Combined calcium chloride and heat treatment delays softening of fresh-cut jackfruit by activating the Ca2+ signaling-NAC29 transcriptional regulatory module.

Fresh-cut jackfruit is highly susceptible to rapid softening during storage, representing a major quality deterioration that limits its commercial distribution. This study elucidated the potential mechanisms by which combined calcium chloride and heat treatment (CH) mitigates softening in fresh-cut jackfruit. CH treatment mitigated cell wall degradation, inhibited the accumulation of water-soluble pectin (WSP), and delayed the degradation of chelator-soluble pectin (CSP) and cellulose, while significantly suppressing the activities of key cell wall-degrading enzymes, including polygalacturonase (PG) and pectin methylesterase (PME). In addition, CH treatment increased Ca2+ content and intracellular accumulation, elevated calmodulin (CaM) levels, and maintained higher Ca2+-ATPase activity. Furthermore, CH treatment reduced the respiration and ethylene biosynthesis. Integrated transcriptomic and WGCNA analyses suggested a putative downstream transcriptional regulatory module associated with the CH treatment response. Among the identified genes, NAC29, C3H, and ERF062 were identified as the key regulatory hubs that potentially translate Ca2+ signals into cell wall stabilization responses. Specifically, we propose a putative model in which a NAC29-centered regulatory module coordinates the expression of key structural genes (such as PE, EG134, and CESAG2), thereby simultaneously promoting cellulose synthesis and inhibiting pectin degradation. These findings provide new insights into the mechanisms by which CH treatment delays softening in fresh-cut jackfruit, providing a theoretical basis for developing effective postharvest preservation strategies.