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Abscisic acid (ABA) is a phytohormone essential for plants to respond to various environmental stresses, and abscisic acid-insensitive 5 (ABI5) is a basic leucine zipper transcription factor of the ABA signaling pathway. Exogenous ABA induces cold tolerance in bananas; however, the role of MaABI5-like in ABA-induced cold tolerance remains unexplored. The present study found that exogenous ABA alleviated chilling injury of ‘Fenjiao’ banana, induced the accumulation of endogenous ABA, unsaturated fatty acids, and flavonoid content, and reduced the saturated fatty acid content. Moreover, ABA treatment up-regulated the transcription levels of MaABI5-like, fatty acid desaturation genes, and flavonoid synthesis-related genes during cold storage. More interestingly, MaABI5-like directly interacted with the promoter of genes related to fatty acid desaturation (MaFAD3-1, MaFAD3-4, MaFAD3-5, MaFAD6-2, MaFAD6-3) and flavonoid synthesis (MaPAL-like, MaPAL-like1, MaC4H-like3, Ma4CL-like1, Ma4CL-like10, MaCHS6-4-like, and MaFLS) and activated their expressions. Furthermore, the transient overexpression of MaABI5-like in ‘Fenjiao’ banana fruit and the ectopic expression in the tomato plants enhanced the cold tolerance and up-regulated fatty acid desaturation and flavonoid synthesis-related gene transcript levels. The reduced expression of MaABI5-like by virus induced gene silencing (VIGS) in ‘Fenjiao’ banana increased the chilling injury and down-regulated the expression of fatty acid desaturation and flavonoid synthesis-related genes. Thus, the study indicates that MaABI5-like regulates ABA-induced cold tolerance by increasing unsaturated fatty acid and flavonoid content.

Banana is a typical subtropical fruit, sensitive to chilling injuries and prone to softening disorder. However, the underlying regulatory mechanisms of the softening disorder caused by cold stress remain obscure. Herein, we found that BEL1‐LIKE HOMEODOMAIN transcription factor 1 (MaBEL1) and its associated proteins regulate the fruit softening and ripening process. The transcript and protein levels of MaBEL1 were up‐regulated with fruit ripening but severely repressed by the chilling stress. Moreover, the MaBEL1 protein interacted directly with the promoters of the cell wall and starch degradation‐related genes, such as MaAMY3, MaXYL32, and MaEXP‐A8. The transient overexpression of MaBEL1 alleviated fruit chilling injury and ripening disorder caused by cold stress and promoted fruit softening and ripening of “Fenjiao” banana by inducing ethylene production and starch and cell wall degradation. The accelerated ripening was also validated by the ectopic overexpression in tomatoes. Conversely, MaBEL1‐silencing aggravated the chilling injury and ripening disorder and repressed fruit softening and ripening by inhibiting ethylene production and starch and cell wall degradation. MaABI5‐like and MaEBF1, the two positive regulators of the fruit softening process, interacted with MaBEL1 to enhance the promoter activity of the starch and cell wall degradation‐related genes. Moreover, the F‐box protein MaEBF1 does not modulate the degradation of MaBEL1, which regulates the transcription of MaABI5‐like protein. Overall, we report a novel MaBEL1‐MaEBF1‐MaABI5‐like complex system that mediates the fruit softening and ripening disorder in “Fenjiao” bananas caused by cold stress.

Ethylene response factors (ERFs) are one of largest plant-specific transcription factor families involved in fruit ripening. However, the regulatory mechanism by which ERFs modulate fruit yellowing and softening remains unknown in banana. We previously found that the transcription of MaERF012 was closely related to ‘Fenjiao’ banana fruit ripening. Herein, we found that MaERF012 was differentially expressed in the fruit pulp and peel and was closely related to fruit ripening. MaERF012 activated the promoter activity of one chlorophyll degradation gene (MaSGR1), two starch degradation genes (MaGWD1 and MaAMY3), and three cell wall degradation genes (MaPL8, MaEXP-A8, and MaXYL23-like), which were tested by EMSA, Y1H, and DLR. Transient overexpression of MaERF012 accelerates fruit ripening by promoting fruit yellowing and softening by up-regulating the transcription of chlorophyll, starch, and cell wall degradation genes. Over-expression of MaERF012 alters the transcriptome profiles of the fruit peel and pulp, and the differentially expressed genes were mainly enriched in starch and sucrose metabolism, plant hormone signal transduction, biosynthesis of secondary metabolism, and fructose and mannose metabolism. Overall, the data showed that MaERF012 acts as a transcriptional activator by regulating fruit ripening by activating the transcription of chlorophyll, starch, and cell wall degradation genes.

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