Replant failure caused by negative plant-soil feedback (NPFS) in agricultural ecosystems is a critical factor restricting the development of sustainable agriculture. Soil nutrient availability has the capacity to affect plant-soil feedback. Here, we used sanqi (Panax notoginseng), which is severely threatened by NPSF, as a model plant to decipher the overall effects of nitrogen (N) rates on NPSF and the underlying mechanism. We found that a high rate of N at 450kgNha (450N) aggravated the NPSF through the accumulation of pathogens in the soil compared with the optimal 250N. The increased N rates resulted in a significant increase in the soil electrical conductivity and available nitrogen but a decrease in the soil pH and C/N ratio. GeoChip 5.0 data demonstrated that these changed soil properties caused the soil to undergo stress (acidification, salinization and carbon starvation), as indicated by the enriched soil microbial gene abundances related to stress response and nutrition cycling (N, C and S). Accordingly, increased N rates reduced the richness and diversity of soil fungi and bacteria and eventually caused a shift in soil microbes from a bacterial-dominant community to a fungal-dominant community. In particular, the high 450N treatment significantly suppressed the abundance of copiotrophic bacteria, including beneficial genera Bacillus and Pseudomonas, thus weakening the antagonistic activity of these bacteria against fungal pathogens. Moreover, 450N application significantly enriched the abundance of pathogen pathogenicity-related genes. Once sanqi plants were grown in this N-stressed soil, their host-specific fungal pathogen Fusarium oxysporum significantly accumulated, which aggravated the process of NPSF. This study suggested that over-application of nitrogen is not beneficial for disease management or the reduction of fungicide application in agricultural production.
There is a concerted understanding of the accumulation of soil pathogens as the major driving factor of negative plant-soil feedback (NPSF). However, our knowledge of the connection between plant growth, pathogen build-up and soil microbiome assemblage is limited. In this study, significant negative feedback between the soil and sanqi ( Panax notoginseng ) was found, which were caused by the build-up of the soil-borne pathogens Fusarium oxysporum , F. solani , and Monographella cucumerina . Soil microbiome analysis revealed that the rhizospheric fungal and bacterial communities were changed with the growth of sanqi. Deep analysis of the phylum and genus levels corroborated that rhizospheric fungal Ascomycota, including the soil-borne pathogens F. oxysporum , F. solani , and especially M. cucumerina , were significantly enriched with the growth of sanqi. However, the bacteria Firmicutes and Acidobacteria, including the genera Pseudomonas , Bacillus, Acinetobacter and Burkholderia , were significantly suppressed with the growth of sanqi. Using microbial isolation and in vitro dual culture tests, we found that most isolates derived from the suppressed bacterial genera showed strong antagonistic ability against the growth of sanqi soil-borne pathogens. Interestingly, inoculation of these suppressed isolates in consecutively cultivated soil could significantly alleviate NPSF. In summary, sanqi growth can suppress antagonistic bacteria through re-assemblage of the rhizosphere microbiome and cause the accumulation of soil-borne pathogens, eventually building negative feedback loops between the soil and plants.
Panax notoginseng (Burk.) F.H. Chen (2n = 2x = 24, common name sanqi or tianqi), belonging to the Araliaceae family, is a slow-growing plant species documented in the ancient Chinese medical literatures for its ability to ameliorate hemostasis and improve blood circulation (Wang et al., 2016). After decades of pharmacological research, a variety of P. notoginseng-specific secondary metabolites (notably ginsenosides, notoginsenosides and gypenosides) were isolated, identified, and implicated in conferring medicinal properties (Wang et al., 2016). These discoveries allowed the design and production of numerous modern oral and topical drugs to treat cardiovascular diseases, contusions, and soft tissue pain (Wang et al., 2016). To help identify novel bioactive compounds in P. notoginseng and delineate their biosynthetic pathways, we propose the construction of a reference P. notoginseng genome. This information will be an important addition to the existing expressed sequence tag (Luo et al., 2011) and RNA-seq data (Liu et al., 2015) for P. notoginseng genetics. J.Z. is an employee and shareholder of NOWBIO Technology Co. Ltd. Y.L. is an employee and shareholder of Longjing Pharmaceutical Co. Ltd. L.Z. is an employee and shareholder of Farlong Pharmaceutical. This work is not financially supported by the abovementioned companies. The three companies took no roles in acquiring or interpreting the results of this manuscript. No conflict of interest declared.
Panax notoginseng is a highly valuable medicinal herb, but its culture is strongly hindered by replant failure, mainly due to autotoxicity. Deciphering the response mechanisms of plants to autotoxins is critical for overcoming the observed autotoxicity. Here, we elucidated the response of P. notoginseng to the autotoxic ginsenoside Rg1 via transcriptomic and cellular approaches. Cellular analyses demonstrated that Rg1 inhibited root growth by disrupting the cell membrane and wall. Transcriptomic analyses confirmed that genes related to the cell membrane, cell wall decomposition and reactive oxygen species (ROS) metabolism were up-regulated by Rg1 stress. Further cellular analyses revealed that Rg1 induced ROS (O2·- and H2O2) accumulation in root cells by suppressing ascorbate peroxidase (APX) and the activities of enzymes involved in the ascorbate-glutathione (ASC-GSH) cycle. Exogenous antioxidants (ASC and gentiobiose) helped cells scavenge over-accumulated ROS by promoting superoxide dismutase (SOD) activity and the ASC-GSH cycle. Collectively, the autotoxin Rg1 caused root cell death by inducing the over-accumulation of ROS, and the use of exogenous antioxidants could represent a strategy for overcoming autotoxicity.
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