Ulrich Louisa, Schmitz Johanna, Thurow Corinna, Gatz Christiane
Department of Plant Molecular Biology and Physiology, Albrecht-von-Haller Institute for Plant Sciences, University of Göttingen, Julia-Lermontowa-Weg 3, 37077 Göttingen, Germany.
J Exp Bot. 2025 May 27;76(8):2356-2372. doi: 10.1093/jxb/eraf056.
Verticillium longisporum is a soil-borne fungal pathogen that causes vascular disease predominantly in Brassicaceae. We have previously reported that the receptor of the plant defense hormone jasmonoyl-isoleucine (JA-Ile), CORONATINE INSENSITIVE 1 (COI1), is required in roots for the fungus to proliferate efficiently in the shoot, suggesting the presence of a mobile root-borne signal that influences the outcome of the disease in shoots. This function of COI1 in promoting susceptibility is independent of JA-Ile. To explore the underlying mechanisms, in this study we compared the root transcriptome of the Arabidopsis coi1 mutant with those of the susceptible JA-Ile-deficient allene oxide synthase (aos) mutant and the susceptible wild-type (WT). The biggest difference between the transcriptomes was due to 316 immunity-related genes that were constitutively higher expressed in coi1 as compared to the susceptible genotypes. Interfering with the expression of a sub-group of these genes partially suppressed the coi1-mediated tolerance phenotype. We therefore hypothesize that secreted defense compounds encoded by genes constitutively expressed in coi1 are transported to the shoot with the transpiration stream where they accumulate and interfere with fungal growth. In addition, we found that 149 of the 316 COI1-repressed genes were induced in the WT and aos upon infection, reaching similar expression levels as in mock-treated coi1. These were not further induced in coi1 upon infection. Thus, the repressive effect of COI1 is either lifted or overridden upon infection with V. longisporum.
长孢轮枝菌是一种土传真菌病原体,主要在十字花科植物中引起维管束疾病。我们之前报道过,植物防御激素茉莉酰异亮氨酸(JA-Ile)的受体冠菌素不敏感1(COI1)在根中是真菌在地上部高效增殖所必需的,这表明存在一种可移动的根源信号,它会影响地上部疾病的发生结果。COI1的这种促进易感性的功能独立于JA-Ile。为了探究其潜在机制,在本研究中,我们比较了拟南芥coi1突变体与易感的JA-Ile缺陷型丙二烯氧化物合酶(aos)突变体和易感野生型(WT)的根转录组。转录组之间最大的差异在于,与易感基因型相比,coi1中有316个免疫相关基因组成型高表达。干扰这些基因的一个亚组的表达部分抑制了coi1介导的耐受性表型。因此,我们推测,由coi1中组成型表达的基因编码的分泌型防御化合物随着蒸腾流运输到地上部,在那里积累并干扰真菌生长。此外,我们发现,在野生型和aos中,316个被COI1抑制的基因中有149个在感染后被诱导,其表达水平与模拟处理的coi1相似。在感染长孢轮枝菌后,coi1中的这些基因没有进一步被诱导。因此,COI1的抑制作用在感染长孢轮枝菌后要么被解除,要么被克服。