Department of Biological Sciences, University of North Texas, Denton, Texas 76203, USA.
Plant Physiol. 2012 Apr;158(4):1860-72. doi: 10.1104/pp.112.193417. Epub 2012 Feb 21.
The Arabidopsis (Arabidopsis thaliana) lipase-like protein PHYTOALEXIN DEFICIENT4 (PAD4) is essential for defense against green peach aphid (GPA; Myzus persicae) and the pathogens Pseudomonas syringae and Hyaloperonospora arabidopsidis. In basal resistance to virulent strains of P. syringae and H. arabidopsidis, PAD4 functions together with its interacting partner ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) to promote salicylic acid (SA)-dependent and SA-independent defenses. By contrast, dissociated forms of PAD4 and EDS1 signal effector-triggered immunity to avirulent strains of these pathogens. PAD4-controlled defense against GPA requires neither EDS1 nor SA. Here, we show that resistance to GPA is unaltered in an eds1 salicylic acid induction deficient2 (sid2) double mutant, indicating that redundancy between EDS1 and SID2-dependent SA, previously reported for effector-triggered immunity conditioned by certain nucleotide-binding-leucine-rich repeat receptors, does not explain the dispensability of EDS1 and SID2 in defense against GPA. Mutation of a conserved serine (S118) in the predicted lipase catalytic triad of PAD4 abolished PAD4-conditioned antibiosis and deterrence against GPA feeding, but S118 was dispensable for deterring GPA settling and promoting senescence in GPA-infested plants as well as for pathogen resistance. These results highlight distinct molecular activities of PAD4 determining particular aspects of defense against aphids and pathogens.
拟南芥（Arabidopsis thaliana）脂肪酶样蛋白 PHYTOALEXIN DEFICIENT4（PAD4）对于防御绿桃蚜（GPA；Myzus persicae）和病原体丁香假单胞菌和葫芦科疫霉至关重要。在对丁香假单胞菌和葫芦科疫霉强毒株的基础抗性中，PAD4与其相互作用伙伴增强疾病易感性 1（EDS1）一起发挥作用，以促进水杨酸（SA）依赖性和 SA 非依赖性防御。相比之下，PAD4 和 EDS1 的分离形式可针对这些病原体的无毒菌株发出效应物触发的免疫信号。PAD4 控制对 GPA 的防御既不需要 EDS1 也不需要 SA。在这里，我们表明，eds1 salicylic acid induction deficient2（sid2）双突变体对 GPA 的抗性没有改变，表明 EDS1 和 SID2 依赖性 SA 之间的冗余性，先前曾报道过某些核苷酸结合亮氨酸重复受体触发的免疫所产生的效应物，不能解释 EDS1 和 SID2 在防御 GPA 方面的非必要性。PAD4 预测的脂肪酶催化三联体中保守丝氨酸（S118）的突变使 PAD4 条件下的抗菌作用和对 GPA 取食的威慑作用丧失，但 S118 对于阻止 GPA 定居和促进受 GPA 侵害的植物衰老以及抵御病原体是可有可无的。这些结果突出了 PAD4 的不同分子活性，这些活性决定了对蚜虫和病原体防御的特定方面。
