Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, College of Agriculture and Life Sciences, Mississippi State, MS, 39762, USA.
Department of Entomology and Plant Pathology, Auburn University, 209 Life Science Building, Auburn, AL, 36849, USA.
Plant Physiol Biochem. 2018 Aug;129:331-348. doi: 10.1016/j.plaphy.2018.06.020. Epub 2018 Jun 18.
Soybean (Glycine max) infection by the charcoal rot (CR) ascomycete Macrophomina phaseolina is enhanced by the soybean cyst nematode (SCN) Heterodera glycines. We hypothesized that G. max genetic lines impairing infection by M. phaseolina would also limit H. glycines parasitism, leading to resistance. As a part of this M. phaseolina resistance process, the genetic line would express defense genes already proven to impair nematode parasitism. Using G. max, exhibiting partial resistance to M. phaseolina, experiments show the genetic line also impairs H. glycines parasitism. Furthermore, comparative studies show G. max exhibits induced expression of the effector triggered immunity (ETI) gene NON-RACE SPECIFIC DISEASE RESISTANCE 1/HARPIN INDUCED1 (NDR1/HIN1) that functions in defense to H. glycines as compared to the H. glycines and M. phaseolina susceptible line G. max. Other defense genes that are induced in G. max include the pathogen associated molecular pattern (PAMP) triggered immunity (PTI) genes ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1), NONEXPRESSOR OF PR1 (NPR1) and TGA2. These observations link G. max defense processes that impede H. glycines parasitism to also potentially function toward impairing M. phaseolina pathogenicity. Testing this hypothesis, G. max genetically engineered to experimentally induce GmNDR1-1, EDS1-2, NPR1-2 and TGA2-1 expression leads to impaired M. phaseolina pathogenicity. In contrast, G. max engineered to experimentally suppress the expression of GmNDR1-1, EDS1-2, NPR1-2 and TGA2-1 by RNA interference (RNAi) enhances M. phaseolina pathogenicity. The results show components of PTI and ETI impair both nematode and M. phaseolina pathogenicity.
大豆（Glycine max）感染炭腐病（CR）子囊菌旋孢腔菌（Macrophomina phaseolina）会被大豆胞囊线虫（SCN）异皮线虫（Heterodera glycines）增强。我们假设，损害旋孢腔菌感染的大豆遗传系也会限制异皮线虫的寄生，从而产生抗性。作为旋孢腔菌抗性过程的一部分，该遗传系会表达已被证明损害线虫寄生的防御基因。使用对旋孢腔菌表现出部分抗性的大豆进行实验表明，该遗传系也会损害异皮线虫的寄生。此外，比较研究表明，与异皮线虫和旋孢腔菌易感系大豆相比，大豆表现出效应触发免疫（ETI）基因 NON-RACE SPECIFIC DISEASE RESISTANCE 1/HARPIN INDUCED1（NDR1/HIN1）的诱导表达，该基因在防御异皮线虫方面起作用。在大豆中诱导表达的其他防御基因包括病原体相关分子模式（PAMP）触发免疫（PTI）基因 ENHANCED DISEASE SUSCEPTIBILITY1（EDS1）、PR1 非表达（NPR1）和 TGA2。这些观察结果将阻碍异皮线虫寄生的大豆防御过程与可能损害旋孢腔菌致病性的过程联系起来。为了验证这一假设，我们对大豆进行了基因工程改造，实验诱导 GmNDR1-1、EDS1-2、NPR1-2 和 TGA2-1 的表达，导致旋孢腔菌致病性受损。相比之下，通过 RNA 干扰（RNAi）实验抑制 GmNDR1-1、EDS1-2、NPR1-2 和 TGA2-1 表达的大豆工程改造增强了旋孢腔菌的致病性。结果表明，PTI 和 ETI 的组成部分损害了线虫和旋孢腔菌的致病性。
