Data from: Plastic transcriptomes stabilize immunity to pathogen diversity: the jasmonic acid and salicylic acid networks within the Arabidopsis/Botrytis pathosystem

To respond to pathogen attack, selection and associated evolution has led to the creation of plant immune system that are a highly effective and inducible defense system. Central to this system are the plant defense hormones jasmonic acid (JA) and salicylic acid (SA) and crosstalk between the two, which may play an important role in defense responses to specific pathogens or even genotypes. Here, we used the Arabidopsis-B. cinerea pathosystem to test how the host's defense system functions against genetic variation in a pathogen. We measured defense-related phenotypes and transcriptomic responses in Arabidopsis wild-type Col-0 and JA- and SA-signaling mutants, coi1-1 and npr1-1, individually challenged with 96 diverse B. cinerea isolates. Those data showed genetic variation in the pathogen influences on all components within the plant defense system at the transcriptional level. We identified four gene co-expression networks and two vectors of defense variation triggered by genetic variation in B. cinerea. This showed that the JA and SA signaling pathways functioned to constrain/canalize the range of virulence in the pathogen population, but the underlying transcriptomic response was highly plastic. These data showed that plants utilize major defense hormone pathways to buffer disease resistance, but not the metabolic or transcriptional responses to genetic variation within a pathogen.

为抵御病原物侵染，经自然选择与协同演化，植物形成了一套高效且可诱导的免疫系统。该系统的核心组分包括植物防卫激素茉莉酸（jasmonic acid, JA）与水杨酸（salicylic acid, SA），以及二者间的激素交叉对话，这一过程可能在针对特定病原物甚至特定基因型的防卫反应中发挥重要作用。本研究以拟南芥-灰葡萄孢（Arabidopsis-B. cinerea）病害互作系统为模型，探究寄主防卫系统如何响应病原物的遗传变异：我们以96株遗传多样性各异的灰葡萄孢菌株分别接种拟南芥野生型Col-0、茉莉酸信号通路突变体coi1-1与水杨酸信号通路突变体npr1-1，并测定了相关防卫表型与转录组应答特征。上述实验数据表明，病原物的遗传变异会在转录组层面影响植物防卫系统的所有组分；我们共鉴定出4个基因共表达网络，以及由灰葡萄孢遗传变异引发的两类防卫变异维度。研究结果显示，茉莉酸与水杨酸信号通路能够约束并稳定病原种群的毒力范围，但其背后的转录组应答却具有高度可塑性；本研究数据证实，植物可通过主要防卫激素通路来缓冲病害抗性，但无法调控针对病原物内部遗传变异的代谢或转录组应答。