The effect of exogenous melatonin on chilling injury in peach fruit after harvest was investigated. To explore the optimum concentration of melatonin for chilling tolerance induction, peach fruit were treated with 50, 100, or 200 μM melatonin for 120 min and then stored for 28 days at 4 °C. The results showed that application of melatonin at 100 μM was most effective in reducing chilling injury of peach fruit after harvest. Peaches treated with melatonin at this concentration displayed higher levels of extractable juice rate and total soluble solids than the non-treated peaches. In addition, melatonin treatment enhanced expression of PpADC, PpODC, and PpGAD and consequently increased polyamines and γ-aminobutyric acid (GABA) contents. Meanwhile, the upregulated transcripts of PpADC and PpODC and inhibited PpPDH expression resulted in the higher proline content in melatonin-treated fruit compared to the control fruit. Our results revealed that melatonin treatment may be a useful technique to alleviate chilling injury in cold-stored peach fruit. The chilling tolerance of harvested peaches induced by melatonin treatment is associated with higher levels of polyamine, GABA, and proline. These data provided here are the first protective evidence of exogenous melatonin in harvested horticultural products in response to direct chilling stress.
Linoleic acid (LA; C18:2) and α-linolenic acid (ALA; C18:3) are two essential unsaturated fatty acids that play indispensable roles in maintaining membrane integrity in cold stress, and ω-3 fatty acid desaturases (FADs) are responsible for the transformation of LA into ALA. However, how this process is regulated at transcriptional and posttranscriptional levels remains largely unknown. In this study, an MYB transcription factor, MaMYB4, of a banana fruit was identified and found to target several ω-3 MaFADs, including MaFAD3-1, MaFAD3-3, MaFAD3-4 and MaFAD3-7, and repress their transcription. Intriguingly, the acetylation levels of histones H3 and H4 in the promoters of ω-3 MaFADs were elevated in response to cold stress, which was correlated with the enhancement in the transcription levels of ω-3 MaFADs and the ratio of ALA/LA. Moreover, a histone deacetylase MaHDA2 physically interacted with MaMYB4, thereby leading to the enhanced MaMYB4-mediated transcriptional repression of ω-3 MaFADs. Collectively, these data demonstrate that MaMYB4 might recruit MaHDA2 to repress the transcription of ω-3 MaFADs by affecting their acetylation levels, thus modulating fatty acid biosynthesis. Our findings provided new molecular insights into the regulatory mechanisms of fatty acid biosynthesis in cold stress in fruits.
Low temperatures are known to destroy cell membranes’ structural integrity by affecting the remodeling of their phospholipids. Fruits stored at low temperature are prone to chilling injury, characterized by discoloration, absence of ripening, surface pitting, growth inhibition, flavor loss, decay, and wilting. Phosphatidic acid, a vital second-messenger lipid in plants, is known to accumulate in response to different kinds of stress stimuli. However, the regulatory mechanism of its production from the degradation of phospholipids remains poorly understood. We identified two cold-responsive NAC (NAM/ATAF1/CUC2) transcription factors from bananas, namely, MaNAC25 and MaNAC28, which negatively regulated cold tolerance in banana fruits by upregulating the expression of phospholipid degradation genes in banana fruits. Furthermore, MaNAC25 and MaNAC28 formed a positive feedback loop to induce phospholipid degradation and produce phosphatidic acid. In contrast, ethylene directly inhibited the degradation of phospholipids in banana and transgenic tomato fruits. In addition, ethylene reduced the activity of MaNAC25 and MaNAC28, thereby inhibiting phospholipid degradation. To conclude, NAC-mediated membrane lipid remodeling negatively regulates the cold tolerance of banana and transgenic tomato fruits.
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