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Effects of phenylpropanoid and energetic metabolism inhibition on faba bean resistance mechanisms to rust.

机译:苯丙烷和能量代谢抑制对蚕豆抗锈作用机理的影响。

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Effects on penetration and hypersensitive resistance of the cinnamyl acid dehydrogenase (CAD) suicide inhibitor ([(2-hydroxyphenyl) amino] sulphinyl) acetic acid, 1.1 dimethyl ester, which suppresses phenylpropanoid biosynthesis, and of D-mannose, which sequesters phosphate and reduces energy available in host cells, were studied in faba bean (Vicia faba) genotypes with differing resistance mechanisms to faba bean rust (Uromyces viciae-fabae). Inhibition of CAD reduced penetration resistance in lines 2N-34, 2N-52, V-1271, and V-1272, revealing an important role for phenylpropanoid biosynthesis in the resistance of these lines. Inhibition of CAD also inhibited hypersensitive cell death in these lines. D-mannose had little or no effect on resistance. By contrast, CAD inhibition did not affect penetration resistance of line BPL-261, which has a high degree of penetration resistance not associated with hypersensitive cell death. In BPL-261, D-mannose inhibited penetration resistance. The parallelism between the faba bean genotype responses to rust observed here and the response of barley genotypes with differing resistance mechanisms to powdery mildew after similar inhibitor treatments is analyzed and discussed.
机译:肉桂酸脱氢酶(CAD)自杀抑制剂([[(2-羟苯基)氨基]亚磺酰基)乙酸,抑制二苯丙烷生物合成的1.1二甲基酯和D-甘露糖的渗透和抗过敏性的影响在蚕豆锈病抗性机制不同的蚕豆(蚕豆)基因型中研究了宿主细胞中可用的能量。 CAD的抑制降低了2N-34、2N-52,V-1271和V-1272品系中的抗穿透性,从而揭示了苯丙烷类生物合成在这些品系的抗性中的重要作用。抑制CAD还可以抑制这些细胞系中的超敏细胞死亡。 D-甘露糖对抗性几乎没有影响。相比之下,CAD抑制作用不会影响BPL-261品系的抗穿透性,该品系具有高度的抗穿透性,与超敏细胞死亡无关。在BPL-261中,D-甘露糖抑制了抗穿透性。分析和讨论了类似的抑制剂处理后,蚕豆基因型对锈病的响应与大麦基因型对白粉病的抗性机制不同的响应之间的平行性。

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