Center for Plant Molecular Biology, Eberhard Karls University of Tübingen, 72076 Tübingen, Germany.
Plant J. 2011 Jun;66(5):818-30. doi: 10.1111/j.1365-313X.2011.04546.x. Epub 2011 Apr 4.
In plants, autophagy has been assigned 'pro-death' and 'pro-survival' roles in controlling programmed cell death associated with microbial effector-triggered immunity. The role of autophagy in basal immunity to virulent pathogens has not been addressed systematically, however. Using several autophagy-deficient (atg) genotypes, we determined the function of autophagy in basal plant immunity. Arabidopsis mutants lacking ATG5, ATG10 and ATG18a develop spreading necrosis upon infection with the necrotrophic fungal pathogen, Alternaria brassicicola, which is accompanied by the production of reactive oxygen intermediates and by enhanced hyphal growth. Likewise, treatment with the fungal toxin fumonisin B1 causes spreading lesion formation in atg mutant genotypes. We suggest that autophagy constitutes a 'pro-survival' mechanism that controls the containment of host tissue-destructive microbial infections. In contrast, atg plants do not show spreading necrosis, but exhibit marked resistance against the virulent biotrophic phytopathogen, Pseudomonas syringae pv. tomato. Inducible defenses associated with basal plant immunity, such as callose production or mitogen-activated protein kinase activation, were unaltered in atg genotypes. However, phytohormone analysis revealed that salicylic acid (SA) levels in non-infected and bacteria-infected atg plants were slightly higher than those in Col-0 plants, and were accompanied by elevated SA-dependent gene expression and camalexin production. This suggests that previously undetected moderate infection-induced rises in SA result in measurably enhanced bacterial resistance, and that autophagy negatively controls SA-dependent defenses and basal immunity to bacterial infection. We infer that the way in which autophagy contributes to plant immunity to different pathogens is mechanistically diverse, and thus resembles the complex role of this process in animal innate immunity.
在植物中，自噬被分配了“促死亡”和“促存活”的角色，以控制与微生物效应子触发的免疫相关的程序性细胞死亡。然而，自噬在植物对毒性病原体的基础免疫中的作用尚未得到系统的研究。使用几种自噬缺陷(atg)基因型，我们确定了自噬在植物基础免疫中的功能。缺乏 ATG5、ATG10 和 ATG18a 的拟南芥突变体在感染坏死性真菌病原体交链孢菌时会发生扩散性坏死，这伴随着活性氧中间体的产生和菌丝生长的增强。同样，用真菌毒素腐霉素 B1 处理也会导致 atg 突变体基因型形成扩散性损伤。我们认为自噬构成了一种“促存活”机制，控制宿主组织破坏性微生物感染的控制。相比之下，atg 植物不会发生扩散性坏死，但对毒性生物营养型植物病原体丁香假单胞菌 pv.番茄表现出明显的抗性。与基础植物免疫相关的诱导防御，如胼胝质的产生或丝裂原激活蛋白激酶的激活，在 atg 基因型中没有改变。然而，植物激素分析显示，非感染和细菌感染的 atg 植物中的水杨酸(SA)水平略高于 Col-0 植物，并且伴随着 SA 依赖的基因表达和 camalexin 产生的升高。这表明以前未检测到的中度感染诱导的 SA 升高导致可测量的增强的细菌抗性，并且自噬负调控 SA 依赖的防御和对细菌感染的基础免疫。我们推断，自噬对不同病原体的植物免疫的贡献方式在机制上是不同的，因此类似于该过程在动物先天免疫中的复杂作用。
