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.

为应对病原菌侵染，自然选择与协同演化催生了植物免疫系统——这是一套高效且可诱导的防御系统。该系统的核心为植物防御激素茉莉酸（jasmonic acid, JA）与水杨酸（salicylic acid, SA），以及二者间的交叉对话，其在针对特定病原菌甚至特定基因型的防御应答中可能发挥关键作用。本研究采用拟南芥-灰葡萄孢（Botrytis cinerea, B. cinerea）病理互作体系，探究宿主防御系统如何应对病原菌的遗传变异。我们以拟南芥野生型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为材料，分别接种96株遗传多样性丰富的灰葡萄孢菌株，检测其防御相关表型与转录组应答。上述数据表明，病原菌的遗传变异会在转录层面影响植物防御系统的所有组分。本研究鉴定出4个基因共表达网络，以及两类由灰葡萄孢遗传变异触发的防御变异途径。该结果揭示，茉莉酸与水杨酸信号通路可约束/定向调控病原菌种群的毒力范围，但下游转录组应答具有高度可塑性。本研究数据表明，植物通过核心防御激素通路维持病害抗性的稳定性，但无法缓冲针对病原菌遗传变异的代谢与转录组应答。