Xu Yadi, Wei He, Li Haixiao, Zeng Fanli, Liu Ning, Cao Zhiyan, Dong Jingao
State Key Laboratory of North China Crop Improvement and Regulation/Hebei Key Laboratory of Plant Physiology and Molecular Pathology, Baoding, China.
College of Life Sciences, Hebei Agricultural University, Baoding, China.
Mol Plant Pathol. 2025 Jun;26(6):e70090. doi: 10.1111/mpp.70090.
Salicylic acid (SA) plays a crucial role in the defence strategies of plants against fungal pathogens. To circumvent plant immunity, pathogens use metabolic enzymes such as salicylate hydroxylase to degrade SA, thereby facilitating successful pathogenicity after infection. This phenomenon has not been previously reported in Cochliobolus heterostrophus. Our study demonstrates that high concentrations of SA can inhibit both growth and spore germination; however, at concentrations below 1 mM, SA does not significantly impact the growth and spore germination of C. heterostrophus, which is capable of metabolising exogenously supplied SA. Transcriptome and LC-MS analyses indicated that C. heterostrophus metabolises exogenous SA via the gentisic acid (GA) pathway, involving genes such as 5-salicylate hydroxylase (ChnagG). Prokaryotic expression of ChnagG confirmed its ability to convert SA into GA. Additionally, we created ChnagG gene deletion and complementation mutants, revealing that ChnagG influences melanin synthesis and the pathogenicity of C. heterostrophus. Analysis of the SA signalling pathway in plants during fungal infection indicated that the ChnagG knockout mutant did not alter the synthesis of SA in its host maize; however, it led to the upregulation of the downstream signalling pathway ZmPR1 gene compared to the wild type. These findings suggest that C. heterostrophus obstructs the immune signalling pathway of maize through SA metabolism, thereby enhancing its infection and pathogenicity. This study lays the groundwork for further elucidating the mechanisms underlying the interaction between maize and C. heterostrophus.
水杨酸(SA)在植物抵御真菌病原体的防御策略中起着关键作用。为了规避植物免疫,病原体利用代谢酶如水杨酸羟化酶来降解SA,从而在感染后促进成功致病。这种现象此前尚未在玉米大斑病菌中报道。我们的研究表明,高浓度的SA可以抑制生长和孢子萌发;然而,在浓度低于1 mM时,SA对能够代谢外源SA的玉米大斑病菌的生长和孢子萌发没有显著影响。转录组和液相色谱-质谱分析表明,玉米大斑病菌通过龙胆酸(GA)途径代谢外源SA,涉及5-水杨酸羟化酶(ChnagG)等基因。ChnagG的原核表达证实了其将SA转化为GA的能力。此外,我们创建了ChnagG基因缺失和互补突变体,发现ChnagG影响玉米大斑病菌的黑色素合成和致病性。对真菌感染期间植物中SA信号通路的分析表明,ChnagG基因敲除突变体不会改变其寄主玉米中SA的合成;然而,与野生型相比,它导致下游信号通路ZmPR1基因上调。这些发现表明,玉米大斑病菌通过SA代谢阻碍玉米的免疫信号通路,从而增强其感染性和致病性。本研究为进一步阐明玉米与玉米大斑病菌相互作用的机制奠定了基础。