The plant stress hormone salicylic acid (SA) participates in local and systemic acquired resistance, which eventually leads to whole-plant resistance to bacterial pathogens. However, if SA-mediated signaling is not appropriately controlled, plants incur defense-associated fitness costs such as growth inhibition and cell death. Despite its importance, to date only a few components counteracting the SA-primed stress responses have been identified in Arabidopsis (Arabidopsis thaliana). These include other plant hormones such as jasmonic acid and abscisic acid, and proteins such as LESION SIMULATING DISEASE1, a transcription coregulator. Here, we describe PLANT NATRIURETIC PEPTIDE A (PNP-A), a functional analog to vertebrate atrial natriuretic peptides, that appears to antagonize the SA-mediated plant stress responses. While loss of PNP-A potentiates SA-mediated signaling, exogenous application of synthetic PNP-A or overexpression of PNP-A significantly compromises the SA-primed immune responses. Moreover, we identify a plasma membrane–localized receptor-like protein, PNP-R2, that interacts with PNP-A and is required to initiate the PNP-A–mediated intracellular signaling. In summary, our work identifies a peptide and its putative cognate receptor as counteracting both SA-mediated signaling and SA-primed cell death in Arabidopsis.

植物应激激素水杨酸（SA）参与局部和系统获得性抗性，最终导致全植物对细菌病原体的抗性。然而，如果 SA 介导的信号传导没有得到适当的控制，植物就会产生与防御相关的适应性成本，例如生长抑制和细胞死亡。尽管其很重要，但迄今为止，在拟南芥中仅发现了少数抵消 SA 引发的应激反应的成分。其中包括其他植物激素，如茉莉酸和脱落酸，以及蛋白质，如 LESION SIMULATING DISEASE1（一种转录共调节因子）。在这里，我们描述了植物钠尿肽 A (PNP-A)，它是脊椎动物心房钠尿肽的功能类似物，似乎可以拮抗 SA 介导的植物应激反应。虽然 PNP-A 的缺失会增强 SA 介导的信号传导，但合成 PNP-A 的外源应用或 PNP-A 的过度表达会显着损害 SA 引发的免疫反应。此外，我们还发现了一种质膜定位的受体样蛋白 PNP-R2，它与 PNP-A 相互作用，并且是启动 PNP-A 介导的细胞内信号传导所必需的。总之，我们的工作确定了一种肽及其假定的同源受体，可以抵消拟南芥中 SA 介导的信号传导和 SA 引发的细胞死亡。