No abstract

The plant hormone ethylene is important for the ripening of climacteric fruit, such as pear (Pyrus ussuriensis), and the brassinosteroid (BR) class of phytohormones affects ethylene biosynthesis during ripening via an unknown molecular mechanism. Here, we observed that exogenous BR treatment suppressed ethylene production and delayed fruit ripening, whereas treatment with a BR biosynthesis inhibitor promoted ethylene production and accelerated fruit ripening in pear, suggesting BR is a ripening suppressor. The expression of the transcription factor BRASSINAZOLE-RESISTANT 1PuBZR1 was enhanced by BR treatment during pear fruit ripening. PuBZR1 interacted with PuACO1, which converts 1-aminocyclopropane-1-carboxylic acid (ACC) to ethylene, and suppressed its activity. BR-activated PuBZR1 bound to the promoters of PuACO1 and of PuACS1a, which encodes ACC synthase, and directly suppressed their transcription. Moreover, PuBZR1 suppressed the expression of transcription factor PuERF2 by binding its promoter, and PuERF2 bound to the promoters of PuACO1 and PuACS1a. We concluded that PuBZR1 indirectly suppresses the transcription of PuACO1 and PuACS1a through its regulation of PuERF2. Ethylene production and expression profiles of corresponding apple (Malus domestica) homologs showed similar changes following epibrassinolide treatment. Together, these results suggest that BR-activated BZR1 suppresses ACO1 activity and the expression of ACO1 and ACS1, thereby reducing ethylene production and suppressing fruit ripening. This likely represents a conserved mechanism by which BR suppresses ethylene biosynthesis during climacteric fruit ripening.

Apple (Malus domestica) is, globally, one of the largest fruits in terms of cultivated area and yield. Apple fruit is generally marketed after storage, which is of great significance for regulating the market supply in the off-season of fruit production. Apple-fruit ripening, which culminates in desirable changes in structural and textural properties, is governed by a complex regulatory network. Much is known about ethylene as one of the most important factors promoting apple-fruit ripening. However, the dynamic interplay between phytohormones also plays an important part in apple-fruit ripening. Here, we review and evaluate the complex regulatory network concerning the action of phytohormones during apple-fruit ripening. Interesting future research areas are discussed.

Nitric oxide (NO) is known to modulate the action of several phytohormones. This includes the gaseous hormone ethylene, but the molecular mechanisms underlying the effect of NO on ethylene biosynthesis are unclear.Here, we observed a decrease in endogenous NO abundance during apple (Malus domestica) fruit development and exogenous treatment of apple fruit with a NO donor suppressed ethylene production, suggesting that NO is a ripening suppressor.Expression of the transcription factor MdERF5 was activated by NO donor treatment. NO induced the nucleocytoplasmic shuttling of MdERF5 by modulating its interaction with the protein phosphatase, MdPP2C57. MdPP2C57-induced dephosphorylation of MdERF5 at Ser260 is sufficient to promote nuclear export of MdERF5. As a consequence of this export, MdERF5 proteins in the cytoplasm interacted with and suppressed the activity of MdACO1, an enzyme that converts 1-aminocyclopropane-1-carboxylic acid (ACC) to ethylene. The NO-activated MdERF5 was observed to increase in abundance in the nucleus and bind to the promoter of the ACC synthase gene MdACS1 and directly suppress its transcription.Together, these results suggest that NO-activated nucleocytoplasmic MdERF5 suppresses the action of ethylene biosynthetic genes, thereby suppressing ethylene biosynthesis and limiting fruit ripening.

During ripening, fleshy fruits undergo irreversible changes in color, texture, sugar content, aroma, and flavor to appeal to seed-dispersal vectors. The onset of climacteric fruit ripening is accompanied by an ethylene burst. Understanding the factors triggering this ethylene burst is important for manipulating climacteric fruit ripening. Here, we review the current understanding and recent insights into the possible factors triggering climacteric fruit ripening: DNA methylation and histone modification, including methylation and acetylation. Understanding the initiation factors of fruit ripening is important for exploring and accurately regulating the mechanisms of fruit ripening. Lastly, we discuss the potential mechanisms responsible for climacteric fruit ripening.

• The dynamic interplay between phytohormones plays an important part in climacteric fruit ripening. • Transcription factors are critical for the regulation of climacteric fruit ripening. • Epigenetic modifications act as important regulators of fruit ripening.

The plant hormone ethylene is important for the ripening of climacteric fruit, such as pear (Pyrus ussuriensis), and the brassinosteroid (BR) class of phytohormones affects ethylene biosynthesis during ripening, although via an unknown molecular mechanism. Here, we observed that exogenous BR treatment suppressed ethylene production during pear fruit ripening, and that the expression of the transcription factor PuBZR1 was enhanced by epibrassinolide (EBR) treatment during pear fruit ripening. PuBZR1 was shown to interact with PuACO1, which converts 1-aminocyclopropane-1-carboxylic acid (ACC) to ethylene, and suppress its activity. We also observed that BR-activated PuBZR1 bound to the promoters of PuACO1 and of PuACS1a, which encodes ACC synthase, and directly suppressed their transcription. Moreover, PuBZR1 suppressed the expression of transcription factor PuERF2 by binding its promoter, and PuERF2 bound to the promoters of PuACO1 and PuACS1a. We concluded that PuBZR1 indirectly suppresses the transcription of PuACO1 and PuACS1a through its regulation of PuERF2. Ethylene production and the expression profiles of the corresponding apple (Malus domestica) homologs showed similar changes following EBR treatment. Together, these results suggest that BR-activated BZR1 suppresses ACO1 activity and the expression of ACO1 and ACS1a, thereby reducing ethylene production during pear and apple fruit ripening. This likely represents a conserved mechanism by which exogenous BR suppresses ethylene biosynthesis during climacteric fruit ripening.One-sentence summaryBR-activated BZR1 suppresses ACO1 activity and expression of ACO1 and ACS1a, which encode two ethylene biosynthesis enzymes, thereby reducing ethylene production during pear and apple fruit ripening.