Gray mold, Botrytis cinerea, infects over 200 plant species and has significant impact on the agriculture industry, yearly >$10 billion of crop lost worldwide due to this pathogenic fungus. Currently the treatment for B. cinerea is spraying plants with fungicide and the annual cost of is estimated to be >$1 billion globally (DeLong et al., 2020) adding to the economic burden. Unfortunately, due to its rapid lifecycle and overuse of fungicides, this pathogenic fungus has a high tendency of developing fungicide resistance therefore, multiple fungicide classes are often combined to treat crops thereby creating a vicious circle. Fungicide exposure (inhalation and ingestion) also has an impact on public health and is associated with an increased risk of cancer and neurological-related diseases. Taken together, there is a critical need to identify other treatment options to combat crop losses without the added health risk.
The KP may play a crucial role in iron acquisition in B. cinerea by linking tryptophan metabolism to siderophore production and redox balance. Siderophores help the fungus obtain iron, but its release requires a reducing environment. The KP generates NAD⁺, which supports redox reactions, potentially aiding iron mobilization. Additionally, the KP enzyme TDO has been linked to siderophore biosynthesis in bacteria, suggesting a similar role in B. cinerea.
In a recently published study, Dr. Li and colleagues investigated the role of another KP rate-limiting enzyme, kynurenine monooxygenase (KMO), in B. cinerea pathogenicity. Using known sequence data of KMO (human and yeast), the researchers identified BcKMO-like sequence (BcKMOL) in a strain of B. cinerea. BcKMOL expression increases transiently during pathogenic growth, suggesting that the KP may play a role in growth. Indeed, mutants lacking BcKMOL had significantly stunted growth and morphological changes compared to WT fungi. Furthermore, the pathogenicity of B. cinerea depends partially on BcKMOL. Mutants lacking BcKMOL produce significantly smaller lesions on tobacco leaves than the WT or mutants with restored BcKMOL. Many of the pathogenic genes associated with penetrating plant cells are significantly reduced in the BcKMOL mutant. Taken together, these data suggest that the KP of B. cinerea plays a role in both pathogenicity and growth, sparking the question of whether targeting BcKMOL is a safe and effective alternative to fungicide treatment.
The researchers used BcKMOL protein to identify potential antimicrobial peptides capable of interacting with BcKMOL. Two peptides, CAMPQ3966 and CAMPQ4589, were further analyzed in this study. Wild type B. cinerea growth was significantly reduced when treated with either CAMPQ3966 or CAMPQ4589 but had no effect on the BcKMOL lacking mutant. Furthermore, application of the antimicrobial peptides to tobacco leaves, apples, and pears significantly reduces the lesion area. While these peptides were successful in limiting fungal growth, the length of these peptides poses challenges for large-scale production in agriculture. However, investing in molecular tools to inhibit the KP may pave the way for safer antifungal solutions.