Abeysekara Nilwala S, Swaminathan Sivakumar, Desai Nalini, Guo Lining, Bhattacharyya Madan K
Department of Agronomy, Iowa State University, Ames, IA, USA; Department of Plant Pathology and Microbiology, Iowa State University, Ames, IA, USA.
Department of Agronomy, Iowa State University, Ames, IA, USA.
Plant Sci. 2016 Feb;243:105-14. doi: 10.1016/j.plantsci.2015.11.008. Epub 2015 Nov 28.
The causal agent of the soybean sudden death syndrome (SDS), Fusarium virguliforme, remains in infected roots and secretes toxins to cause foliar SDS. In this study we investigated the xylem sap, roots, and leaves of F. virguliforme-infected and -uninfected soybean seedlings for any changes in a set of over 3,000 metabolites following pathogen infection by conducting GC/MS and LC/MS/MS, and detected 273 biochemicals. Levels of many intermediates of the TCA cycle were reduced suggesting suppression of this metabolic pathway by the pathogen. There was an increased accumulation of peroxidated lipids in leaves of F. virguliforme-infected plants suggesting possible involvement of free radicals and lipoxygenases in foliar SDS development. Levels of both isoflavone conjugates and isoflavonoid phytoalexins were decreased in infected roots suggesting degradation of these metabolites by the pathogen to promote root necrosis. The levels of the plant immunity inducer pipecolic acid (Pip) and the plant hormone salicylic acid (SA) were significantly increased in xylem sap (in case of Pip) and leaves (in case of both Pip and SA) of F. virguliforme-infected soybean plants compared to the control plants. This suggests a major signaling role of Pip in inducing host defense responses in above ground parts of the F. virguliforme-infected soybean. Increased accumulation of pipecolic acid in foliar tissues was associated with the induction of GmALD1, the soybean homolog of Arabidopsis ALD1. This metabolomics study generated several novel hypotheses for studying the mechanisms of SDS development in soybean.
大豆猝死综合征（SDS）的致病因子——尖孢镰刀菌，会残留在受感染的根部并分泌毒素，从而引发叶片的SDS症状。在本研究中，我们通过气相色谱/质谱联用（GC/MS）和液相色谱/串联质谱联用（LC/MS/MS），对受尖孢镰刀菌感染和未感染的大豆幼苗的木质部汁液、根和叶进行检测，以研究在病原体感染后3000多种代谢物中的任何变化，并检测到273种生化物质。三羧酸循环的许多中间产物水平降低，这表明病原体抑制了该代谢途径。在受尖孢镰刀菌感染的植物叶片中，过氧化脂质积累增加，这表明自由基和脂氧合酶可能参与了叶片SDS的发展。在受感染的根中，异黄酮共轭物和异黄酮植保素的水平均降低，这表明病原体降解了这些代谢物，从而促进根坏死。与对照植物相比，在受尖孢镰刀菌感染的大豆植物的木质部汁液（就哌啶酸而言）和叶片（就哌啶酸和水杨酸而言）中，植物免疫诱导剂哌啶酸（Pip）和植物激素水杨酸（SA）的水平显著增加。这表明Pip在诱导受尖孢镰刀菌感染的大豆地上部分的宿主防御反应中起主要信号作用。叶片组织中哌啶酸积累的增加与拟南芥ALD1的大豆同源物GmALD1的诱导有关。这项代谢组学研究为研究大豆SDS发生机制提出了几个新的假设。
