Li Bai, Zhang Kang, Wang Jialin, Zhai Siqi, Cao Hongzhe, Si Helong, Zang Jinping, Xing Jihong, Dong Jingao
State Key Laboratory of North China Crop Improvement and Regulation, Hebei Agricultural University, Baoding 071000, China; Hebei Key Laboratory of Plant Physiology and Molecular Pathology, Hebei Agricultural University, Baoding 071000, China; College of Plant Protection, Hebei Agricultural University, Baoding 071000, China.
State Key Laboratory of North China Crop Improvement and Regulation, Hebei Agricultural University, Baoding 071000, China; Hebei Key Laboratory of Plant Physiology and Molecular Pathology, Hebei Agricultural University, Baoding 071000, China; College of Life Science, Hebei Agricultural University, Baoding 071000, China.
Microbiol Res. 2025 Oct;299:128243. doi: 10.1016/j.micres.2025.128243. Epub 2025 May 28.
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.
犬尿氨酸途径最初是在哺乳动物中被发现的。它是色氨酸分解代谢的主要途径，参与许多重要的生物学过程，是神经退行性疾病治疗的一个靶点。然而，该途径及其功能在灰葡萄孢中尚未见报道。在本研究中，通过生物信息学分析获得了与犬尿氨酸途径相关的基因BcIDO、BcKFA、BcHAO、BcKYN、BcKMO和BcKAT。BcKYNL1和BcKYNL2基因突变体对灰葡萄孢的生长、致病性及应激反应具有正向调控作用。对突变体△BcKYNL1和△BcKYNL2中犬尿氨酸途径关键代谢产物的分析表明，突变体中色氨酸代谢相关产物的含量发生了显著变化。外源添加喹啉酸部分恢复了突变体的致病性。这些结果表明，BcKYNL1和BcKYNL2通过影响犬尿氨酸途径的代谢物含量来调节致病性。此外，分子对接和表面离子共振分析确定，犬尿氨酸酶BcKYNL1和BcKYNL2分别直接作用于犬尿氨酸途径的犬尿氨酸和3-羟基犬尿氨酸，且由BcKYNL2和BcKMO调控的分支是犬尿氨酸途径的主要分支。这些结果为犬尿氨酸途径调控灰葡萄孢生长和致病性的机制以及灰葡萄孢防治新靶点的开发与应用提供了新的见解。
