Septoria gentianae prompts both systemic-induced susceptibility and systemic acquired resistance targeting specific pathognes

Plants and pathogens fight each other not only on pathogen-infected leaves but also on non-infected systemic leaves. Systemic acquired resistance (SAR) is a well-known plant defense system during pathogen infection. In contrast, current reports showed that primary infections of some fungal or bacterial pathogens systemically enhance host susceptibility for their following infection, which is termed systemic-induced susceptibility (SIS). Here, we found that Septoria gentianae (Sg), a fungal pathogen of gentians, systemically induces SIS in gentian plants by increasing the number of host stomata, the entry sites of this fungus, in newly-developed leaves. Expression of a fungal candidate secreted effector-like protein, Rapid Alkalinization Factor (SgRALF) homologous to a plant peptide hormone, and its gentian homolog led to increased stomatal density in gentian plants, suggests that SgRALF could hijack and manipulate the host mechanism controlling stomatal development to promote the secondary infection of Sg via increasing stomatal density. Interestingly, Sg infection leads to the expression of SAR-related genes and induces the resistance to another pathogen in the systemic leaves where the SIS to Sg occurs at the same time. In addition, we found that SIS signaling candidate prevent the effect of salicylic acid on stomatal development, suggesting that SIS and SAR signals may compete with each other, but cause SIS or SAR to specific pathogens at the same time.