Effect of Phosphate-Deficiency Stress on the Biological Characteristics and Transcriptomics of Panax ginseng

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The low availability of phosphorus has become a common problem worldwide. Phosphorus is essential for phenotypic morphology and ginsenoside synthesis. However, the effects of Pi stress on ginseng phenotype and ginsenoside synthesis remain unclear. Phenotypic analyses and transcriptomics revealed the phenotypic construction and regulation of differential genes involved in the physiological metabolism of ginseng under low-Pi stress. Root length and stem length were found to be significantly inhibited by phosphate-deficiency stress in the half-phosphate (HP) and no-phosphate (NP) treatment groups; however, the number of fibrous roots, which are regulated by phytohormones, was found to increase. In ginseng leaves, the indexes of physiological stress, superoxide anion (221.19 nmol/g) and malonaldehyde (MDA) (0.05 μmol/min/g), reached the maximum level. Moreover, chlorophyll fluorescence images and chlorophyll content further confirmed the inhibition of ginseng photosynthesis under low-Pi stress. A total of 579 and 210 differentially expressed genes (DEGs) were shared between NP and total phosphate (TP) and HP and TP, respectively, and only 64 common DEGs were found based on the two comparisons. These DEGs were mainly related to the synthesis of phosphate transporters (PHTs), phytohormones, and ginsenosides. According to KEGG analyses, four DEGs (Pg_s 0368.2, Pg_s3418.1, Pg_s5392.5 and Pg_s3342.1) affected acetyl-CoA production by regulating glycometabolism and tricarboxylic acid cycle (TCA). In addition, related genes, including those encoding 13 PHTs, 15 phytohormones, and 20 ginsenoside synthetases, were screened in ginseng roots under Pi-deficiency stress. These results indicate that changes in the ginseng phenotype and transcriptional regulation of DEGs are involved in the Pi-deficiency stress environment of ginseng, thereby providing new information regarding the development of ginseng for low-Pi tolerance.

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