Abstract
During postharvest life, broccoli suffers from floret yellowing confining its economic and nutritional value. The objective of the present study was to explore the mechanisms employed by phytosulfokine α (PSKα) at 150 nM for delaying floret yellowing in broccoli during storage at 4°C for 28 days. Our results showed that the higher endogenous accumulation of hydrogen sulfide (H2S) resulting from the higher gene expression and activities of l-cysteine desulfhydrase (LCD) and d-cysteine desulfhydrase (DCD) in broccoli floret treated with 150 nM PSKα may serve as an endogenous signaling molecule for delaying senescence. Moreover, the suppressed ethylene biosynthesis in broccoli floret treated with 150 nM PSKα might be ascribed to lower gene expression and activities of ACC synthase (ACS) and ACC oxidase (ACO). Furthermore, lower gene expression and activities of Mg2+ dechelatase (MDC), pheophytinase (PPH), and pheophorbide a oxygenase (PaO) might be the reasons for the higher accumulation of chlorophyll in broccoli floret treated with 150 nM PSKα. Based on our findings, exogenous PSKα application could be employed as signaling bioactive hormone for retarding floret yellowing of broccoli during storage at 4°C for 28 days.
Highlights
The present study aimed to investigate the connection between exogenous phytosulfokine α (PSKα) application and broccoli floret yellowing and elucidate its mechanisms from the perspective of endogenous H2S accumulation by L-cysteine desulfhydrase (LCD) and D-cysteine desulfhydrase (DCD) gene expressions and enzyme activities, chlorophyll degradation by Mg2+ dechelatase (MDC), PPH, and pheophorbide a oxygenase (PaO) gene expressions, and enzyme activities accompanied by ethylene biosynthesis by ACC synthase (ACS) and ACC oxidase (ACO) gene expressions and enzyme activities by employing exogenous PSKα application at 0 and 150 nM during storage at 4◦C for 28 days
Retarding floret yellowing in broccoli treated with PSKα at 150 nM was concomitant with lower ethylene production (P < 0.01; Figure 1), which might be attributed to lower ACS1 and ACO1 gene expressions and enzyme activities (P < 0.01; Figure 1) during storage at 4◦C for 28 days
Higher ethylene biosynthesis by ACS and ACO gene expressions and enzyme activities may be the reason for triggering floret yellowing in broccoli by promoting membrane phospholipids degradation by phospholipase D (PLD) gene expression and enzyme activity leading to free fatty acids supplying for peroxidation by LOX gene expression and enzyme activity
Summary
Owing to higher health-promoting bioactive molecules accumulation, broccoli has gained worldwide attention as a global healthy food crop, which is beneficial for ensuring human health by reducing the risk of chronic diseases, such as cancer, cardiovascular diseases, and neurodegenerative diseases in industrial countries [1].By harvesting broccoli prematurely, a high accumulation of intracellular reactive oxygen species (ROS) [2], an insufficient intracellular supply of ATP [3, 4], an imbalance of intracellular hormones, signified by a higher biosynthesis of ethylene and a lower biosynthesis of cytokinin [5, 6], and chlorophyll degradation via the pheophorbide a oxygenase (PaO) pathway [2, 6,7,8,9] may be the mechanisms for the accelerated broccoli senescence, manifested by floret yellowing, which confines its commercial value. There are ongoing attempts to introduce safe and operative procedures for avoiding floret yellowing and preserving the floret quality of broccoli during cold storage
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