在矮牵牛丛枝菌根共生过程中,VAPYRIN通过抑制PR基因诱导和局部木质素积累来减弱防御作用

Min Chen, Sébastien Bruisson, Laure Bapaume, Geoffrey Darbon, G. Glauser, M. Schorderet, D. Reinhardt
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引用次数: 11

摘要

在丛枝菌根(AM)共生中,宿主和真菌的密切联系可能引发宿主对真菌的防御机制的诱导,这意味着成功的共生需要抑制防御。我们通过在矮牵牛(Petunia hybrida)中使用am缺陷的vapyrin (vpy)突变体来解决这一现象,包括一个新的等位基因(vpy-3),该等位基因在ATG起始密码子附近插入转座子。我们探讨了真菌感染在vpy突变体中的流产是否与防御标记的诱导有关,如细胞壁改变、活性氧(ROS)的积累、防御激素和致病相关(PR)基因的诱导。我们发现,vpy突变体对细胞内定植具有很强的抵抗力,这与木质素浸渍真菌进入位点产生厚细胞壁附着(乳头)有关,而没有观察到防御激素、活性氧或胼胝质的积累。对PR基因表达的系统分析表明,在野生型菌根中有几种PR基因被诱导,而在vvy植物中更多。一些PR基因只在vpy突变体中被诱导。综上所述,这些结果表明,VPY参与避免或抑制细胞防御综合征的诱导,该综合征涉及局部木质素沉积和PR基因诱导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida
The intimate association of host and fungus in arbuscular mycorrhizal (AM) symbiosis can potentially trigger induction of host defence mechanisms against the fungus, implying that successful symbiosis requires suppression of defence. We addressed this phenomenon by using AM-defective vapyrin (vpy) mutants in Petunia hybrida, including a new allele (vpy-3) with a transposon insertion close to the ATG start codon. We explore whether abortion of fungal infection in vpy mutants is associated with the induction of defence markers such as cell wall alterations, accumulation of reactive oxygen species (ROS), defence hormones, and induction of pathogenesis-related (PR) genes. We show that vpy mutants exhibit a strong resistance against intracellular colonization, which is associated with the generation of thick cell wall appositions (papillae) with lignin impregnation at fungal entry sites, while no accumulation of defence hormones, ROS, or callose was observed. Systematic analysis of PR gene expression revealed that several PR genes are induced in mycorrhizal roots of the wild type, and even more in vpy plants. Some PR genes are induced exclusively in vpy mutants. Taken together, these results suggest that VPY is involved in avoiding or suppressing the induction of a cellular defence syndrome that involves localized lignin deposition and PR gene induction.
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