Abstract
Fruit ripening in response to propylene (an ethylene analog), 1-methylcyclopropene (1-MCP, an ethylene action inhibitor), and low temperature (5°C) treatments was characterized in “Kosui” kiwifruit (Actinidia rufa × A. chinensis). Propylene treatment induced ethylene production, with increased expression levels of 1-aminocyclopropane-1-carboxylic acid (ACC) synthase 1 (AcACS1) and ACC oxidase 2 (AcACO2), and rapid fruit softening together with increased expression levels of polygalacturonase (AcPG) and expansin 1 (AcEXP1) within 5 days (d). Fruit soluble solids concentration (SSC) and contents of sucrose, glucose, and fructose together with the expression levels of β-amylase 1 (Acβ-AMY1), Acβ-AMY2, and invertase (AcINV3-1) increased rapidly after 5 d exposure to propylene. Furthermore, propylene exposure for 5 d was sufficient to induce the production of key aroma volatile compounds, ethyl- and methyl butanoate, accompanied with increased expression levels of alcohol acyl transferase (AcAAT). Application of 1-MCP at the start of the experiment, followed by continuous exposure to propylene, significantly delayed fruit softening, changes in SSC and sugars, and strongly suppressed the production of ethylene, aroma volatiles, and expression of associated genes. During storage, fruit softening, SSC and sugar increase, and increased expression of genes associated with cell wall modification and carbohydrate metabolism were registered without detectable ethylene production; however, these changes occurred faster at 5°C compared to 22°C. Interestingly, ethyl and methyl butanoate as well as AcAAT expression were undetectable in kiwifruit during storage, while they were rescued by post-storage propylene exposure, indicating that the production of aroma volatile compounds is strongly ethylene-dependent. Transcript levels of a NAC-related transcription factor (TF), AcNAC3, increased in response to both propylene and low temperature treatments, while AcNAC5 was exclusively up-regulated by propylene. By contrast, transcript levels of a MADS-box TF, AcMADS2, exclusively increased in response to low temperature. The above findings indicate that kiwifruit ripening is inducible by either ethylene or low temperature signals. However, fruit ripened by low temperature were deficient in ethylene-dependent aroma volatiles, suggesting that ethylene signaling is non-functional during low temperature-modulated ripening in kiwifruit. These data provide further evidence that ethylene-dependent and low temperature-modulated ripening in kiwifruit involve different regulatory mechanisms.
Highlights
The plant hormone ethylene regulates a wide range of plant growth and developmental processes, including fleshy fruit ripening (Lashbrook et al, 1998; Giovannoni, 2004)
Our results using “Kosui” kiwifruit are consistent with previous research; fruit softening and the expression of cell wall modification-associated genes were induced during storage at 5◦C (Figure 2), despite the lack of any measurable increase in ethylene production (Figure 1)
The present work strongly suggests that ethylene signaling is non-functional during low temperature-modulated ripening in kiwifruit
Summary
The plant hormone ethylene regulates a wide range of plant growth and developmental processes, including fleshy fruit ripening (Lashbrook et al, 1998; Giovannoni, 2004). Fleshy fruit undergo various physiological, biochemical, and structural changes including softening, starch degradation to sugars, pigment accumulation, and production of aroma volatiles (Klee and Giovannoni, 2011; Osorio et al, 2013). Exogenous ethylene or propylene treatment initiates rapid fruit softening through the induction of several cell wall modification-associated genes such as polygalacturonase (AcPG) and expansin 1 (AcEXP1) (Wang et al, 2000; Atkinson et al, 2011; Mworia et al, 2012). Ethylene-induced ripening changes in kiwifruit are usually followed by a sharp increase in ethylene production caused by the up-regulation of key biosynthetic genes AcACS1 and AcACO2 (Pratt and Reid, 1974; Mworia et al, 2010; Atkinson et al, 2011; McAtee et al, 2015)
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