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在矮牵牛丛枝菌根共生过程中,VAPYRIN通过抑制病程相关基因的诱导和局部木质素积累来削弱防御反应。

VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida.

作者信息

Chen Min, Bruisson Sébastien, Bapaume Laure, Darbon Geoffrey, Glauser Gaëtan, Schorderet Martine, Reinhardt Didier

机构信息

Department of Biology, University of Fribourg, Fribourg, CH-1700, Switzerland.

Neuchâtel Platform of Analytical Chemistry, University of Neuchâtel, Neuchâtel, 2000, Switzerland.

出版信息

New Phytol. 2021 Mar;229(6):3481-3496. doi: 10.1111/nph.17109. Epub 2020 Dec 25.

DOI:10.1111/nph.17109
PMID:33231304
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7986166/
Abstract

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 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. Our 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.

摘要

在丛枝菌根(AM)共生中,宿主与真菌的紧密关联可能会触发宿主针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。我们通过使用矮牵牛中AM缺陷型的vapyrin(vpy)突变体来研究这一现象,其中包括一个新的等位基因(vpy-3),其转座子插入靠近ATG起始密码子。我们探究vpy突变体中真菌感染的中止是否与防御标记物的诱导有关,如细胞壁改变、活性氧(ROS)积累、防御激素以及病程相关(PR)基因的诱导。我们发现vpy突变体对细胞内定殖表现出强烈抗性,这与在真菌侵入位点形成木质素浸渍的细胞壁附着体(乳突)有关,而未观察到防御激素、ROS或胼胝质的积累。对PR基因表达的系统分析表明,一些PR基因在野生型菌根根中被诱导,在vpy植株中诱导程度更高。一些PR基因仅在vpy突变体中被诱导。我们的结果表明,VPY参与避免或抑制涉及局部木质素沉积和PR基因诱导的细胞防御综合征的诱导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/39852d55bd21/NPH-229-3481-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/345fce4bd580/NPH-229-3481-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/97f40c9c377f/NPH-229-3481-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/f954140a7903/NPH-229-3481-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/e58639a486c7/NPH-229-3481-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/39852d55bd21/NPH-229-3481-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/345fce4bd580/NPH-229-3481-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/97f40c9c377f/NPH-229-3481-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/f954140a7903/NPH-229-3481-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/e58639a486c7/NPH-229-3481-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eded/7986166/39852d55bd21/NPH-229-3481-g001.jpg

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