背景回顾：Phosphorylation modification is required for the modulation of phytochrome B (phyB) thermal reversion, but the kinase(s) that phosphorylate(s) phyB and the biological significance of the phosphorylation are still unknown. 

提出问题：Here we report that FERONIA (FER) phosphorylates phyB to regulate plant growth and salt tolerance, and the phosphorylation not only regulates dark-triggered photobody dissociation but also modulates phyB protein abundance in the nucleus. 

结果1-FER磷酸化phyB：Further analysis indicates that phosphorylation of phyB by FER is sufficient to accelerate the conversion of phyB from the active form (Pfr) to the inactive form (Pr). 

结果2-盐胁迫抑制FER：Under salt stress, FER kinase activity is inhibited, leading to delayed photobody dissociation and increased phyB protein abundance in the nucleus. 

结果3-phyB突变：Our data also show that phyB mutation or overexpression of PIF5 attenuates growth inhibition and promotes plant survival under salt stress. 

结论：Together, our study not only reveals a kinase that controls phyB turnover via a signature of phosphorylation, but also provides mechanistic insights into the role of the FER-phyB module in coordinating plant growth and stress tolerance.

磷酸化修饰是调节光敏色素phyB热逆转（thermal reversion）所必需的，但磷酸化phyB的激酶以及这一磷酸化的生物学意义仍不清晰。本文中，作者报道了FER能够磷酸化phyB，以调节植物的生长和盐耐受性，磷酸化不仅调控由黑暗诱导的光小体（photobody）解离，还能够调节核中phyB蛋白的丰度。进一步的分析表明，FER对于phyB的磷酸化足以加速phyB从活性形式（Pfr）向非活性形式（Pr）的转变。在盐胁迫下，FER激酶活性受到抑制，导致光小体解离延迟以及核中phyB蛋白丰度增加。作者的数据还表明，phyB突变或者PIF5过表达减弱了植物在盐胁迫的生长抑制，并促进了植物的存活。总之，本文的研究结果不仅揭示了一种通过磷酸化信号控制phyB周转的激酶，而且还解析了FER-phyB模块在协调植物生长和胁迫抗性中的作用机制。