Albrecht-von-Haller-Institut fuer Pflanzenwissenschaften, Georg-August-Universitaet Goettingen, Untere Karspuele 2, D-37073 Goettingen, Germany.
Plant J. 2010 Jan;61(2):200-10. doi: 10.1111/j.1365-313X.2009.04044.x. Epub 2009 Oct 12.
The three closely related Arabidopsis basic leucine zipper (bZIP) transcription factors TGA2, TGA5 and TGA6 are required for the establishment of the salicylic acid (SA)-dependent plant defense response systemic acquired resistance, which is effective against biotrophic pathogens. Here we show that the same transcription factors are essential for the activation of jasmonic acid (JA)- and ethylene (ET)-dependent defense mechanisms that counteract necrotrophic pathogens: the tga256 triple mutant is impaired in JA/ET-induced PDF1.2 and b-CHI expression, which correlates with a higher susceptibility against the necrotroph Botrytis cinerea. JA/ET induction of the trans-activators ERF1 and ORA59, which act upstream of PDF1.2, was slightly increased (ERF1) or unaffected (ORA59). PDF1.2 expression can be restored in the tga256 mutant by increased expression of ORA59, as observed in the tga256 jin1 quadruple mutant, which lacks the transcription factor JIN1/AtMYC2 that functions as a negative regulator of the JA/ET-dependent anti-fungal defense program. Whereas JA/ET-induced PDF1.2 expression is strongly suppressed by SA in wild-type plants, no negative effect of SA on PDF1.2 expression was observed in the tga256 jin1 quadruple mutant. These results imply that the antagonistic effects of TGA factors and JIN1/AtMYC2 on the JA/ET pathway are necessary to evoke the SA-mediated suppression of JA/ET-induced defense responses.
三个密切相关的拟南芥碱性亮氨酸拉链 (bZIP) 转录因子 TGA2、TGA5 和 TGA6 是建立依赖水杨酸 (SA) 的植物防御反应系统获得性抗性所必需的,这种抗性对生物营养性病原体有效。在这里,我们表明,相同的转录因子对于激活茉莉酸 (JA) 和乙烯 (ET) 依赖的防御机制也是必不可少的,这些机制可以抵抗坏死性病原体:tga256 三重突变体在 JA/ET 诱导的 PDF1.2 和 b-CHI 表达中受损,这与对坏死性病原体 Botrytis cinerea 的更高敏感性相关。JA/ET 诱导的转录激活因子 ERF1 和 ORA59,它们作用于 PDF1.2 的上游,其诱导作用略有增加(ERF1)或不受影响(ORA59)。在 tga256 jin1 四重突变体中,观察到缺失转录因子 JIN1/AtMYC2 的情况下,JIN1/AtMYC2 作为 JA/ET 依赖的抗真菌防御程序的负调控因子,ORA59 的过表达可以恢复 tga256 突变体中的 PDF1.2 表达。虽然在野生型植物中,SA 强烈抑制 JA/ET 诱导的 PDF1.2 表达,但在 tga256 jin1 四重突变体中没有观察到 SA 对 PDF1.2 表达的负效应。这些结果表明,TGA 因子和 JIN1/AtMYC2 对 JA/ET 途径的拮抗作用对于引发 SA 介导的 JA/ET 诱导防御反应的抑制是必要的。