Pathogenesis strategies and regulation of ginsenosides by two species of Ilyonectria in Panax ginseng: power of speciation

BACKGROUND: The valuable medicinal plant Panax ginseng has high pharmaceutical efficacy because it produces ginsenosides. However, its yields decline because of a root-rot disease caused by Ilyonectria mors-panacis. Because species within Ilyonectria showed variable aggressiveness by altering ginsenoside concentrations in inoculated plants, we investigated how such infections might regulate the biosynthesis of ginsenosides and their related signaling molecules. METHODS: Two-year-old ginseng seedlings were treated with I. mors-panacis and I. robusta. Roots from infected and pathogen-free plants were harvested at 4 and 16 days after inoculation. We then examined levels or/and expression of genes of ginsenosides, salicylic acid (SA), jasmonic acid (JA), and reactive oxygen species (ROS). We also checked the susceptibility of those pathogens to ROS. RESULTS: Ginsenoside biosynthesis was significantly suppressed and increased in response to infection by I. mors-panacis and I. robusta, respectively. Regulation of JA was significantly higher in I. robusta–infected roots, while levels of SA and ROS were significantly higher in I. mors-panacis–infected roots. Catalase activity was significantly higher in I. robusta–infected roots followed in order by mock roots and those infected by I. mors-panacis. Moreover, I. mors-panacis was resistant to ROS compared with I. robusta. CONCLUSION: Infection by the weakly aggressive I. robusta led to the upregulation of ginsenoside production and biosynthesis, probably because only a low level of ROS was induced. In contrast, the more aggressive I. mors-panacis suppressed ginsenoside biosynthesis, probably because of higher ROS levels and subsequent induction of programmed cell death pathways. Furthermore, I. mors-panacis may have increased its virulence by resisting the cytotoxicity of ROS.