FERONIA interacts with ABI2-type phosphatases to facilitate signaling cross-talk between abscisic acid and RALF peptide in Arabidopsis
FERONIA interacts with ABI2-type phosphatases to facilitate signaling cross-talk between abscisic acid and RALF peptide in Arabidopsis
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FERONIA 与 ABI2 型磷酸酶相互作用，促进拟南芥中脱落酸和 RALF 肽之间的信号串扰。
DOI：
10.1073/pnas.1608449113
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发表时间：
2016-09-13
影响因子：
11.1
通讯作者：
Luan, Sheng
中科院分区：
文献类型：
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作者：
Chen, Jia;Yu, Feng;Luan, Sheng
受体样激酶Feronia（FER）在植物对小分子激素的反应中起着至关重要的作用[例如生长素和脱落酸（ABA）]和肽信号[例如，快速碱化因子（Ralf）]。 FER如何在控制细胞生长和应力反应的控制中整合这些不同的信号事件仍然未知。在应力条件下，ABA水平的升高将抑制根部的细胞伸长。在我们以前的工作中，我们已经表明，通过激活鸟嘌呤核苷酸交换因子1（GEF1）/4/10-rho植物11（ROP11）途径，增强了磷酸酶ABA不敏感2（ABI2），不敏感2（ABI2），不敏感的活性ABA信号传导的负调节剂，从而抑制ABA响应。在这项研究中，我们发现RALF和ABA都通过增加FER的磷酸化水平而激活了FER。 FER功能丧失突变体对ABA和非生物胁迫（例如盐和寒冷条件）表现出强烈的超敏反应，表明FER在ABA和应力反应中起关键作用。我们进一步表明，ABI2与FER直接相互作用并去磷酸化，从而抑制了FER活性。其他几种ABI2样磷酸酶也在该途径中起作用，ABA依赖性FER激活需要吡霉素耐药性（PYR）/Pyr1-like（PYL）/调节成分ABA受体（RCAR）-A-A-A-A-type蛋白磷酸蛋白磷酸酶2C（PP2CA）（PP2CA） ）模块。此外，抑制RALF1基因表达，类似于FER基因的破坏，使植物对ABA过敏。这些结果制定了ABA激活FER和ABA和肽激素RALF之间的ABA激活机制，以控制植物生长和对应激信号的反应。
Receptor-like kinase FERONIA (FER) plays a crucial role in plant response to small molecule hormones [e.g., auxin and abscisic acid (ABA)] and peptide signals [e.g., rapid alkalinization factor (RALF)]. It remains unknown how FER integrates these different signaling events in the control of cell growth and stress responses. Under stress conditions, increased levels of ABA will inhibit cell elongation in the roots. In our previous work, we have shown that FER, through activation of the guanine nucleotide exchange factor 1 (GEF1)/4/10-Rho of Plant 11 (ROP11) pathway, enhances the activity of the phosphatase ABA Insensitive 2 (ABI2), a negative regulator of ABA signaling, thereby inhibiting ABA response. In this study, we found that both RALF and ABA activated FER by increasing the phosphorylation level of FER. The FER loss-of-function mutant displayed strong hypersensitivity to both ABA and abiotic stresses such as salt and cold conditions, indicating that FER plays a key role in ABA and stress responses. We further showed that ABI2 directly interacted with and dephosphorylated FER, leading to inhibition of FER activity. Several other ABI2-like phosphatases also function in this pathway, and ABA-dependent FER activation required PYRABACTIN RESISTANCE (PYR)/PYR1-LIKE (PYL)/REGULATORY COMPONENTS OF ABA RECEPTORS (RCAR)-A-type protein phosphatase type 2C (PP2CA) modules. Furthermore, suppression of RALF1 gene expression, similar to disruption of the FER gene, rendered plants hypersensitive to ABA. These results formulated a mechanism for ABA activation of FER and for cross-talk between ABA and peptide hormone RALF in the control of plant growth and responses to stress signals.