Abstract

Mitochondrial processes are implicated in plant response to biotic stress caused by viruses, actinomyces, bacteria and pests, but their function in defense against fungal invasion remains unclear. Here, we investigated the role and regulation of mitochondrial alternative oxidase (AOX) in response to black spot disease caused by the hemibiotrophic fungus Marssonina brunnea in poplar. M. brunnea inoculation induced the transcription of the AOX1a gene in the mitochondrial electron transport chain and of jasmonic acid (JA) and ethylene (ET) biosynthetic genes, with the accumulation of these phytohormones in poplar leaf, while inhibiting the transcript amount of the mitochondrial cytochrome c oxidase gene (COX6b) and genes related to salicylic acid (SA). Enhanced AOX reduced poplar susceptibility to M. brunnea with a higher ATP/ADP ratio while the repressed AOX caused the reverse effect. Exogenous JA and 1-aminocyclopropane-1-carboxylic acid (ACC, a biosynthetic precursor of ET) inhibited the transcript amount of COX6b and consequently increased the ratio of AOX pathway to total respiration. Furthermore, the transcription of CYS C1 and CYS D1 genes catalyzing cyanide metabolism was induced, while the cysteine (CYS) substrate levels reduced upon M. brunnea inoculation; exogenous JA and ACC mimicked the effect of M. brunnea infection on cysteine. Exogenous SA enhanced, while JA and ACC reduced, poplar susceptibility to M. brunnea. Moreover, inhibiting AOX completely prohibited JA- and ET-increased tolerance to M. brunnea in poplar. These observations indicate that the JA- and ET-induced mitochondrial AOX pathway triggers defense against M. brunnea in poplar. This effect probably involves cyanide. These findings deepen our understanding of plant–pathogenic fungi interactions.

中文翻译：

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茉莉酸和乙烯诱导的线粒体替代氧化酶刺激白杨的Marssonina brunnea防御。

摘要

线粒体过程涉及植物对由病毒，放线菌，细菌和害虫引起的生物胁迫的响应，但是它们在防御真菌侵袭中的功能仍不清楚。在这里，我们研究了线粒体替代氧化酶（AOX）在响应由半生养真菌真菌Marssonina brunnea引起的黑斑病中的作用和调节。M.褐接种诱导的转录AOX1a基因在线粒体电子传递链和茉莉酸（JA）和乙烯（ET）的生物合成的基因，以在杨树叶植物激素这些的累积，同时抑制线粒体的转录量细胞色素c氧化酶基因（COX6b）以及与水杨酸（SA）相关的基因。增强AOX降低杨树易感性M.褐具有较高的ATP / ADP比而抑制AOX引起相反的效果。外源JA和1-氨基环丙烷-1-羧酸（ACC，ET的生物合成前体）抑制了COX6b的转录量，因此增加了AOX途径与总呼吸的比率。此外，诱导CYS C1和CYS D1基因转录可催化氰化物代谢，而半胱氨酸分枝杆菌接种后半胱氨酸（CYS）底物水平降低。外源JA和ACC模仿了布鲁氏菌半胱氨酸感染。杨树易感布鲁纳氏菌，外源SA增强，而JA和ACC降低。此外，抑制AOX完全禁止了JA和ET增加对杨树布鲁氏杆菌的耐受性。这些观察结果表明，JA和ET诱导的线粒体AOX途径触发了杨树对布鲁氏杆菌的防御。这种作用可能涉及氰化物。这些发现加深了我们对植物与病原性真菌相互作用的理解。