Fruit development
Fleshy fruit texture is a critically important quality characteristic of ripe fruit. Softening is an irreversible process which operates in most fleshy fruits during ripening which, together with changes in color and taste, contributes to improvements in mouthfeel and general attractiveness. Softening results mainly from the expression of genes encoding enzymes responsible for cell wall modifications but starch degradation and high levels of flavonoids can also contribute to texture change. Some fleshy fruit undergo lignification during development and post-harvest, which negatively affects eating quality. Excessive softening can also lead to physical damage and infection, particularly during transport and storage which causes severe supply chain losses. Many transcription factors (TFs) that regulate fruit texture by controlling the expression of genes involved in cell wall and starch metabolism have been characterized. Some TFs directly regulate cell wall targets, while others act as part of a broader regulatory program governing several aspects of the ripening process. In this review, we focus on advances in our understanding of the transcriptional regulatory mechanisms governing fruit textural change during fruit development, ripening and post-harvest. Potential targets for breeding and future research directions for the control of texture and quality improvement are discussed.
The NAC transcription factor NONRIPENING (NOR) is a master regulator of climacteric fruit ripening. Melon (Cucumis melo L.) has climacteric and non-climacteric fruit ripening varieties and is an ideal model to study fruit ripening. Two natural CmNAC-NOR variants, the climacteric haplotype CmNAC-NORS,N and the non-climacteric haplotype CmNAC-NORA,S, have effects on fruit ripening; however, their regulatory mechanisms have not been elucidated. Here, we report that a natural mutation in the transcriptional activation domain of CmNAC-NORS,N contributes to climacteric melon fruit ripening. CmNAC-NOR knockout in the climacteric-type melon cultivar “BYJH” completely inhibited fruit ripening, while ripening was delayed by 5–8 d in heterozygous cmnac-nor mutant fruits. CmNAC-NOR directly activated carotenoid, ethylene, and abscisic acid biosynthetic genes to promote fruit coloration and ripening. Furthermore, CmNAC-NOR mediated the transcription of the “CmNAC-NOR-CmNAC73-CmCWINV2” module to enhance flesh sweetness. The transcriptional activation activity of the climacteric haplotype CmNAC-NORS,N on these target genes was significantly higher than that of the non-climacteric haplotype CmNAC-NORA,S. Moreover, CmNAC-NORS,N complementation fully rescued the non-ripening phenotype of the tomato (Solanum lycopersicum) cr-nor mutant, while CmNAC-NORA,S did not. Our results provide insight into the molecular mechanism of climacteric and non-climacteric fruit ripening in melon.
Sugars are involved in plant growth, fruit quality, and signaling perception. Therefore, understanding the mechanisms involved in soluble sugar accumulation is essential to understand fruit development. Here, we report that MdPFPβ, a pyrophosphate-dependent phosphofructokinase gene, regulates soluble sugar accumulation by enhancing the photosynthetic performance and sugar-metabolizing enzyme activities in apple (Malus domestica Borkh.). Biochemical analysis revealed that a basic helix-loop-helix (bHLH) transcription factor, MdbHLH3, binds to the MdPFPβ promoter and activates its expression, thus promoting soluble sugar accumulation in apple fruit. In addition, MdPFPβ overexpression in tomato influenced photosynthesis and carbon metabolism in the plant. Furthermore, we determined that MdbHLH3 increases photosynthetic rates and soluble sugar accumulation in apple by activating MdPFPβ expression. Our results thus shed light on the mechanism of soluble sugar accumulation in apple leaves and fruit: MdbHLH3 regulates soluble sugar accumulation by activating MdPFPβ gene expression and coordinating carbohydrate allocation.
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