Abstract

The nutritional value of broccoli (Brassica oleracea L. var. Italica), its health benefits, as well as its economic value in world production make broccoli an ideal target for improvement given its current postharvest problems related to rapid senescence. Broccoli florets are harvested when their flowers are still developing and photosynthetically active. Harvest causes disruption of supply of water, hormones, nutrients, and energy, leads to imbalance of source-to-sink transition, and triggers stress-induced senescence. There is a clear gap in knowledge about the mechanisms of developmentally regulated, natural (on-plant) senescence and stress-induced postharvest senescence in broccoli. In this study, we aimed at elucidating the molecular mechanisms of natural (on-plant) senescence in broccoli in contrast to postharvest senescence. The genetic progression of natural senescence in broccoli florets was profiled in this study through the RNA-sequencing approach. Candidate genes were identified at each developmental stage of broccoli floret for the involvement of senescence by developmental signals. We further conducted comparative transcriptome analysis on those genes under developmentally regulated senescence and stress-induced postharvest senescence. We found that many genes behave differently in the two conditions, such as sugar transport family, senescence-associated genes (SAGs), ethylene biosynthesis and signaling genes, and flower senescence genes. A comparison of two SWEET family genes SWEET 3 and SWEET 9 in natural and postharvest senescence demonstrated opposite roles in source-sink transition in broccoli. Moreover, we found previously unreported transcription factors including stomatal patterning genes MUTE, SCREAM2, and FAMA and brassinosteroid signaling gene BR ENHANCED EXPRESSION 1 (BEE) that were regulated during natural senescence. In this research, we identified genes involved in natural senescence and further compared with postharvest senescence of commercial maturity broccoli to understand the dynamic senescence networks regulated by both developmental cues and stress signals.

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