Abstract:

Fruit softening is a critical physiological process that occurs during fruit ripening and senescence. Nitric oxide (NO) and NAM-ATAF1/2-CUC2 (NAC) transcription factors (TFs) have been implicated in regulating fruit softening. However, the functions of NO and NAC-like, activated by apetala3/pistillata (NAP) TFs and their interaction in fruit softening are not well understood. Here, we found that NO might suppress cell wall-related enzyme [polygalacturonase (PG), pectin methyl esterase (PME)] activity, thereby effectively postponing tomato fruit softening. Transcriptome and reverse transcription quantitative PCR (RT-qPCR) analyses revealed SlNAP2 in tomato fruit was repressed by NO. Meanwhile, SlNAP2 promoted tomato fruit softening by increasing PG, PME and cellulase activity and reducing cellulose content. Importantly, NO was not effective in delaying tomato fruit softening in the slnap2 mutant. Furthermore, SlNAP2 enhanced fruit soften-related genes SlPL8, SlPG2a and SlCCEL2 transcription by binding to their promoters. However, NO suppressed the activation of SlNAP2 on these genes. Taken together, NO might delay fruit softening by inhibiting the transcriptional activation of SlNAP2 on SlCCEL2, SlPG2a, and SlPL8 to decrease cellulase, PG and PME activity. Thus, this study provides compelling evidence and new insights into the roles of SlNAP2 in NO-regulated tomato fruit softening.