State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, China.
State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing, China.
PLoS Pathog. 2018 Jan 31;14(1):e1006878. doi: 10.1371/journal.ppat.1006878. eCollection 2018 Jan.
Potassium (K+) is required by plants for growth and development, and also contributes to immunity against pathogens. However, it has not been established whether pathogens modulate host K+ signaling pathways to enhance virulence and subvert host immunity. Here, we show that the effector protein AvrPiz-t from the rice blast pathogen Magnaporthe oryzae targets a K+ channel to subvert plant immunity. AvrPiz-t interacts with the rice plasma-membrane-localized K+ channel protein OsAKT1 and specifically suppresses the OsAKT1-mediated K+ currents. Genetic and phenotypic analyses show that loss of OsAKT1 leads to decreased K+ content and reduced resistance against M. oryzae. Strikingly, AvrPiz-t interferes with the association of OsAKT1 with its upstream regulator, the cytoplasmic kinase OsCIPK23, which also plays a positive role in K+ absorption and resistance to M. oryzae. Furthermore, we show a direct correlation between blast disease resistance and external K+ status in rice plants. Together, our data present a novel mechanism by which a pathogen suppresses plant host immunity by modulating a host K+ channel.
钾（K+）是植物生长和发育所必需的，也有助于增强植物对病原体的免疫力。然而，目前还不清楚病原体是否会调节宿主的 K+信号通路，以增强其毒性并颠覆宿主的免疫能力。在这里，我们发现稻瘟病菌的效应蛋白 AvrPiz-t 靶向一种 K+通道，从而颠覆植物的免疫。AvrPiz-t 与水稻质膜定位的 K+通道蛋白 OsAKT1 相互作用，并特异性抑制 OsAKT1 介导的 K+电流。遗传和表型分析表明，OsAKT1 的缺失会导致 K+含量降低和对稻瘟病菌的抗性降低。引人注目的是，AvrPiz-t 干扰了 OsAKT1 与其上游调节剂细胞质激酶 OsCIPK23 的结合，而 OsCIPK23 也在 K+吸收和对稻瘟病菌的抗性中发挥积极作用。此外，我们还表明，在水稻植株中，稻瘟病抗性与外部 K+状态之间存在直接相关性。总之，我们的数据提供了一种新的机制，即病原体通过调节宿主 K+通道来抑制植物宿主的免疫。
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