Transcriptional Activation and Production of Tryptophan-Derived Secondary Metabolites in Arabidopsis Roots Contributes to the Defense against the Fungal Vascular Pathogen Verticillium longisporum

Transcriptional Activation and Production of Tryptophan-Derived Secondary Metabolites in Arabidopsis Roots Contributes to the Defense against the Fungal Vascular Pathogen Verticillium longisporum
复制标题

DOI:
10.1093/mp/sss044
复制
发表时间:
2012-11-01
期刊:
影响因子:
27.5
通讯作者:
Droege-Laser, Wolfgang
Droege-Laser, Wolfgang
中科院分区:
生物学1区
文献类型:
--
作者:
Iven, Tim;Koenig, Stefanie;Droege-Laser, Wolfgang

文献摘要

被引文献

相似文献

土传真菌病原体长孢黄萎病会导致十字花科寄主植物(如油菜)发生维管束疾病。真菌定植于根木质部,并向上移动到叶子,在那里疾病症状变得可见。使用拟南芥作为早期基因诱导的模型,我们分别针对孢子萌发后立即和根皮层穿透期间的菌丝生长进行了根转录组分析。受感染的根表现出基因表达的快速重编程,例如转录因子、应激和防御相关基因的激活。在这里,我们重点关注高度协调的基因诱导,从而产生色氨酸衍生的次级代谢产物。先前对叶子的研究表明,CYP81F2 和 PEN2 (PENETRATION2) 编码的酶执行抗真菌吲哚芥子油苷 (IGS) 代谢物的形成。在黄萎病感染的根中,我们发现 CYP81F2 和 PEN2 同源物 PEL1 (PEN2-LIKE1) 的转录激活,但抗真菌 IGS 分解产物没有增加。相比之下,吲哚-3-羧酸(I3CA)和植物抗毒素camalexin在受感染的根中积累,但只有camalexin抑制体外黄萎病的生长。虽然导致camalexin或CYP81F2依赖性IGS代谢物的个体代谢途径的遗传破坏不会改变黄萎病引起的疾病症状,但两个分支中受损的cyp79b2 cyp79b3突变体导致易感性显着增强。因此,我们的数据提供了对根特异性早期防御的深入了解,并建议色氨酸衍生的代谢物作为针对血管病原体的活性抗真菌化合物。
The soil-borne fungal pathogen Verticillium longisporum causes vascular disease on Brassicaceae host plants such as oilseed rape. The fungus colonizes the root xylem and moves upwards to the foliage where disease symptoms become visible. Using Arabidopsis as a model for early gene induction, we performed root transcriptome analyses in response to hyphal growth immediately after spore germination and during penetration of the root cortex, respectively. Infected roots showed a rapid reprogramming of gene expression such as activation of transcription factors, stress-, and defense-related genes. Here, we focused on the highly coordinated gene induction resulting in the production of tryptophan-derived secondary metabolites. Previous studies in leaves showed that enzymes encoded by CYP81F2 and PEN2 (PENETRATION2)execute the formation of antifungal indole glucosinolate (IGS) metabolites. In Verticillium-infected roots, we found transcriptional activation of CYP81F2 and the PEN2 homolog PEL1 (PEN2-LIKE1), but no increase in antifungal IGS breakdown products. In contrast, indole-3-carboxylic acid (I3CA) and the phytoalexin camalexin accumulated in infected roots but only camalexin inhibited Verticillium growth in vitro. Whereas genetic disruption of the individual metabolic pathways leading to either camalexin or CYP81F2-dependent IGS metabolites did not alter Verticillium-induced disease symptoms, a cyp79b2 cyp79b3 mutant impaired in both branches resulted in significantly enhanced susceptibility. Hence, our data provide an insight into root-specific early defenses and suggest tryptophan-derived metabolites as active antifungal compounds against a vascular pathogen.