Biotrophy-necrotrophy switch in pathogen evoke differential response in resistant and susceptible sesame involving multiple signaling pathways at different phases

Biotrophy-necrotrophy switch in pathogen evoke differential response in resistant and susceptible sesame involving multiple signaling pathways at different phases
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DOI:
10.1038/s41598-017-17248-7
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发表时间:
2017-12-08
期刊:
影响因子:
4.6
通讯作者:
Kundu, Surekha
Kundu, Surekha
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Chowdhury, Supriyo;Basu, Arpita;Kundu, Surekha

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炭腐真菌Macrophomina phaseolina在芝麻中的感染阶段首次揭示了通过BNS(生物营养到坏死营养转换)从生物营养到坏死营养的转变,这一点通过转录研究得到证实。显微镜下使用正常和GFP表达的病原体表现出典型的收缩厚胞间双营养菌丝,引起薄的细胞内坏死营养菌丝在BNS和这个阶段被推迟在一个抗性主机。结果还表明,随着病原菌感染策略的转变,宿主也会调整其防御策略以适应变化的情况。BNS处理后,ROS积累减少,ROS信号转导基因表达上调,抗氧化酶活性升高,导致抗性。BNS后次级代谢产物积累增多,次级代谢产物相关基因表达上调。在不断变化的感染阶段,在一段时间内监测的总共20个基因在植物防御的不同方面发挥作用,显示出协调的反应。植物激素引发和植物激素抑制剂的实验表明,JA-ET信号通路的激活是导致抗性的原因。最重要的是,这种防御反应在抗性宿主中比在易感宿主中更迅速,表明抗性宿主在感染期间做出与易感宿主不同的选择,这最终影响疾病的严重程度。
Infection stages of charcoal rot fungus Macrophomina phaseolina in sesame revealed for the first time a transition from biotrophy via BNS (biotrophy-to-necrotrophy switch) to necrotrophy as confirmed by transcriptional studies. Microscopy using normal and GFP-expressing pathogen showed typical constricted thick intercellular bitrophic hyphae which gave rise to thin intracellular necrotrophic hyphae during BNS and this stage was delayed in a resistant host. Results also show that as the pathogen switched its strategy of infection, the host tailored its defense strategy to meet the changing situation. Less ROS accumulation, upregulation of ROS signaling genes and higher antioxidant enzyme activities post BNS resulted in resistance. There was greater accumulation of secondary metabolites and upregulation of secondary metabolite-related genes after BNS. A total of twenty genes functioning in different aspects of plant defense that were monitored over a time course during the changing infection phases showed a coordinated response. Experiments using phytohormone priming and phytohormone inhibitors showed that resistance resulted from activation of JA-ET signaling pathway. Most importantly this defense response was more prompt in the resistant than the susceptible host indicating that a resistant host makes different choices from a susceptible host during infection which ultimately influences the severity of the disease.