Ningning Gou

Fruit color affects its commercial value. β-carotene is the pigment that provides color for many fruits and vegetables. However, the molecular mechanism of β-carotene metabolism during apricot ripening is largely unknown. Here, we investigated whether β-carotene content affects apricot fruit color. First, the differences in β-carotene content between orange apricot ‘JTY’ and white apricot ‘X15’ during nine developmental stages (S1–S9) were compared. β-carotene contents highly significantly differed between ‘JTY’ and ‘X15’ from S5 (color transition stage) onwards. Whole-transcriptome analysis showed that the β-carotene synthesis genes 15-cis-phytoene desaturase (PaPDS) and 15-cis-phytoene synthase (PaPSY) significantly differed between the two cultivars during the color transition stage. There was a 5 bp deletion in exon 11 of PaPDS in ‘X15’, which led to early termination of amino acid translation. Gene overexpression and virus-induced silencing analysis showed that truncated PaPDS disrupted the β-carotene biosynthesis pathway in apricot pulp, resulting in decreased β-carotene content and a white phenotype. Furthermore, virus-induced silencing analysis showed that PaPSY was also a key gene in β-carotene biosynthesis. These findings provide new insights into the molecular regulation of apricot carotenoids and provide a theoretical reference for breeding new cultivars of apricot.

The apricot (Prunus armeniaca L.) is a fruit that belongs to the Rosaceae family; it has a unique flavor and is of important economic and nutritional value. The composition and content of soluble sugars and organic acids in fruit are key factors in determining the flavor quality. However, the molecular mechanism of sugar and acid accumulation in apricots remains unclear. We measured sucrose, fructose, glucose, sorbitol, starch, malate, citric acid, titratable acid, and pH, and investigated the transcriptome profiles of three apricots (the high-sugar cultivar ‘Shushanggan’, common-sugar cultivar ‘Sungold’, and low-sugar cultivar ‘F43’) at three distinct developmental phases. The findings indicated that ‘Shushanggan’ accumulates a greater amount of sucrose, glucose, fructose, and sorbitol, and less citric acid and titratable acid, resulting in a better flavor; ‘Sungold’ mainly accumulates more sucrose and less citric acid and starch for the second flavor; and ‘F43’ mainly accumulates more titratable acid, citric acid, and starch for a lesser degree of sweetness. We investigated the DEGs associated with the starch and sucrose metabolism pathways, citrate cycle pathway, glycolysis pathway, and a handful of sugar transporter proteins, which were considered to be important regulators of sugar and acid accumulation. Additionally, an analysis of the co-expression network of weighted genes unveiled a robust correlation between the brown module and sucrose, glucose, and fructose, with VIP being identified as a hub gene that interacted with four sugar transporter proteins (SLC35B3, SLC32A, SLC2A8, and SLC2A13), as well as three structural genes for sugar and acid metabolism (MUR3, E3.2.1.67, and CSLD). Furthermore, we found some lncRNAs and miRNAs that regulate these genes. Our findings provide clues to the functional genes related to sugar metabolism, and lay the foundation for the selection and cultivation of high-sugar apricots in the future.

Fruit size is one of the essential quality traits and influences the economic value of apricots. To explore the underlying mechanisms of the formation of differences in fruit size in apricots, we performed a comparative analysis of anatomical and transcriptomics dynamics during fruit growth and development in two apricot cultivars with contrasting fruit sizes (large-fruit Prunus armeniaca ‘Sungold’ and small-fruit P. sibirica ‘F43’). Our analysis identified that the difference in fruit size was mainly caused by the difference in cell size between the two apricot cultivars. Compared with ‘F43’, the transcriptional programs exhibited significant differences in ‘Sungold’, mainly in the cell expansion period. After analysis, key differentially expressed genes (DEGs) most likely to influence cell size were screened out, including genes involved in auxin signal transduction and cell wall loosening mechanisms. Furthermore, weighted gene co-expression network analysis (WGCNA) revealed that PRE6/bHLH was identified as a hub gene, which interacted with 1 TIR1, 3 AUX/IAAs, 4 SAURs, 3 EXPs, and 1 CEL. Hence, a total of 13 key candidate genes were identified as positive regulators of fruit size in apricots. The results provide new insights into the molecular basis of fruit size control and lay a foundation for future breeding and cultivation of larger fruits in apricot.