Recent research has illustrated that signaling networks, after the plant host perceives diverse pathogen-derived signals, facilitate defense responses through mitogen-activated protein kinase (MAPK) cascades, calcium-dependent protein kinase (CDPK), or receptor-like cytoplasmic kinase (RLCK). The pathogen-induced reactive oxygen species (ROS) burst is mainly caused by activation of an NADPH oxidase, designated as the respiratory burst oxidase homolog (RBOH). Emerging evidence emphasizes that NbRBOHB could be activated by CDPK- or RLCK-dependent phosphorylation in association with the pattern-triggered immunity (PTI)–ROS burst. On the other hand, the effector-triggered immunity (ETI)–ROS burst appears to be regulated by upregulation of NbRBOHB via the MAPK–WRKY pathway, followed by the activation of NbRBOHB through CDPK-mediated phosphorylation.
Rotting of roots and stem bases and wilting of entire plants of gentian (Gentiana triflora Pall.) were found in Tochigi Prefecture in August 2011. A fungus, isolated repeatedly from the diseased plants, was identified as a species belonging to clade 3 of the Fusarium solani species complex based on morphological and molecular analyses. The isolates reproduced the symptoms on gentian plants in an inoculation test and were reisolated from the inoculated plants. In this report, we propose the Japanese name “tachigare-byo” for this root rot disease of gentian caused by a Fusarium sp. belonging to the F. solani species complex.