Kynureninase from Botrytis cinerea regulates the growth, development, pathogenicity, and stress response of B. cinerea through the kynurenine pathway

Abstract

The kynurenine pathway was first identified in mammals. It is the main pathway for tryptophan catabolism, participates in many important biological processes, and is a target for the treatment of neurodegenerative diseases. However, this pathway and its function have not been reported in Botrytis cinerea. In this study, the kynurenine pathway-related genes BcIDO, BcKFA, BcHAO, BcKYN, BcKMO, and BcKAT were obtained by bioinformatics analysis. The BcKYNL1 and BcKYNL2 gene mutants positively regulated the growth and pathogenicity of Botrytis cinerea and the stress response. Analysis of the key metabolites of the kynurenine pathway in the mutants △BcKYNL1 and △BcKYNL2 revealed that the significantly changed contents of tryptophan metabolism-related products in the mutants. The exogenous addition of quinolinic acid partially restored the pathogenicity of the mutants. These results indicate that BcKYNL1 and BcKYNL2 regulate pathogenicity by affecting the metabolite content of the kynurenine pathway. In addition, molecular docking and surface ion resonance analyses determined that the kynurenine enzymes BcKYNL1 and BcKYNL2 directly act on kynurenine and 3-hydroxykynurenine of the kynurenine pathway, respectively, and that the branch regulated by BcKYNL2 and BcKMO is the main branch of the kynurenine pathway. These results provide new insights into the mechanism by which the kynurenine pathway regulates the growth and pathogenicity of Botrytis cinerea and the development and application of new targets for the prevention and treatment of B. cinerea.