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人参与根腐病原菌的相互作用。

Interaction of Ginseng with Root Rot Pathogens.

作者信息

Bischoff Nunes Isadora, Goodwin Paul H

机构信息

School of Environmental Sciences, University of Guelph, 50 Stone Road East, Guelph, ON N1G 2W1, Canada.

出版信息

Plants (Basel). 2022 Aug 19;11(16):2152. doi: 10.3390/plants11162152.

Abstract

The species complex (A.A. Hildebr.) A. Cabral and Crous 2011 contains species of soilborne necrotrophic plant pathogens. The most aggressive to ginseng roots is , whereas , , and are less aggressive. Infected ginseng roots show orange-red to black-brown lesions that can expand into a severe root rot, known as disappearing root rot, where only epidermal root tissue remains. Leaves become red-brown with wilting, and stems can have vascular discoloration with black-brown lesions at the base. Less aggressive species trigger jasmonic acid (JA)-related defenses inducing host ginsenosides, pathogenesis-related (PR) proteins, wound periderm, and cell wall thickening. In contrast, triggers reactive oxygen species (ROS) and salicylic acid (SA) production but suppresses JA-related defenses and ginsenoside accumulation. It is also able to suppress SA-related PR protein production. Virulence factors include potential effectors that may suppress PAMP (Pathogen Associated Molecular Patterns) triggered immunity (PTI), polyphenoloxidases, Hsp90 inhibitors, siderophores and cell-wall-degrading enzymes, such as pectinases. Overall, appears to be more aggressive because it can suppress JA and SA-related PTI allowing for more extensive colonization of ginseng roots. While many possible mechanisms of host resistance and pathogen virulence mechanisms have been examined, there is a need for using genetic approaches, such as RNAi silencing of genes of or , to determine their importance in the interaction.

摘要

物种复合体(A.A. 希尔德布兰德)A. 卡布拉尔和克劳斯于2011年提出,该复合体包含土壤传播的坏死性植物病原体物种。对人参根最具侵袭性的是[具体物种未提及],而[其他物种未提及]的侵袭性较弱。受感染的人参根会出现橙红色至黑褐色的病斑,这些病斑可扩展成严重的根腐病,即所谓的消失性根腐病,此时仅留下根的表皮组织。叶片会变成红棕色并枯萎,茎基部的维管束会变色,出现黑褐色病斑。侵袭性较弱的[具体物种未提及]物种会触发茉莉酸(JA)相关的防御反应,诱导宿主产生人参皂苷、病程相关(PR)蛋白、创伤周皮和细胞壁增厚。相比之下,[具体物种未提及]会引发活性氧(ROS)和水杨酸(SA)的产生,但会抑制JA相关的防御反应和人参皂苷的积累。它还能够抑制SA相关的PR蛋白产生。致病因子包括可能抑制病原体相关分子模式(PAMP)触发的免疫反应(PTI)的潜在效应子、多酚氧化酶、热休克蛋白90抑制剂、铁载体以及细胞壁降解酶,如果胶酶。总体而言,[具体物种未提及]似乎更具侵袭性,因为它可以抑制JA和SA相关的PTI,从而使人参根能够被更广泛地定殖。虽然已经研究了许多宿主抗性和病原体致病机制的可能机制,但仍需要使用遗传方法,如对[具体物种未提及]或[具体物种未提及]的基因进行RNA干扰沉默,以确定它们在相互作用中的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1a6/9416147/38aec4c3319a/plants-11-02152-g001.jpg

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