The agave wilt associated with Fusarium oxysporum (Fox) is a major disease of blue agave (Agave tequilana Weber var. azul), used to produce “Tequila” in Mexico. Little is known about the A. tequilana-F. oxysporum interaction yet understanding defense mechanisms against the pathogen is necessary for control strategies. During early Fox infection, plants trigger defense mechanisms to interrupt the compatible interaction, while Fox’s pathogenesis mechanism interacts with plant response. This study evaluated plant defense mechanisms induced by Fox in A. tequilana and their interaction with fungal pathogenesis. For this, an A. tequilana pathogenic strain (FPA), and the non-A. tequilana pathogenic strains FNPA and FOL were utilized. Early defense mechanisms evaluated were hypersensitive response (HR) and cell wall strengthening in agave roots. Resistance mechanisms evaluated included pathogenesis-related proteins (PR proteins), phytoanticipins and phytoalexins. For early defense, induced HR was greater with FPA than other strains. Cell wall strengthening was found in agave roots, plants responded differentially to different strains. Initial response to FPA and FOL was similar in PR proteins, phytoalexins and phytoanticipins production. However, the response differentiated with FOL over time, indicating an incompatible interaction. The study identified effective and ineffective defense responses of A. tequilana to Fox infection, where FPA exhibited compatibility and caused unregulated ROS and PCD, early inhibition of PR activity, extensive lignification, and saponin detoxification. In contrast, this study unveiled incompatible interactions (FNPA and FOL) because of limited colonization, localized HR with suppressed ROS, early and sustained POX activation, significant callose accumulation, moderate lignification, and phenol–saponin dynamics that help in tissue containment and recovery.
Navarro-López et al. (Mon,) studied this question.