College of Life Sciences, Hunan Normal University, Changsha 410081, People's Republic of China.
Proc Natl Acad Sci U S A. 2012 Sep 4;109(36):14693-8. doi: 10.1073/pnas.1212547109. Epub 2012 Aug 20.
Plant growth and development are controlled by a delicate balance of hormonal cues. Growth-promoting hormones and growth-inhibiting counterparts often antagonize each other in their action, but the molecular mechanisms underlying these events remain largely unknown. Here, we report a cross-talk mechanism that enables a receptor-like kinase, FERONIA (FER), a positive regulator of auxin-promoted growth, to suppress the abscisic acid (ABA) response through activation of ABI2, a negative regulator of ABA signaling. The FER pathway consists of a FER kinase interacting with guanine exchange factors GEF1, GEF4, and GEF10 that, in turn, activate GTPase ROP11/ARAC10. Arabidopsis mutants disrupted in any step of the FER pathway, including fer, gef1gef4gef10, or rop11/arac10, all displayed an ABA-hypersensitive response, implicating the FER pathway in the suppression mechanism. In search of the target for the FER pathway, we found that the ROP11/ARAC10 protein physically interacted with the ABI2 phosphatase and enhanced its activity, thereby linking the FER pathway with the inhibition of ABA signaling.
植物的生长和发育受激素信号的精细平衡调控。促进生长的激素和抑制生长的激素在其作用中常常相互拮抗,但这些事件背后的分子机制在很大程度上仍然未知。在这里,我们报告了一种交叉对话机制,该机制使受体样激酶 FERONIA(FER)能够通过激活 ABA 信号负调节剂 ABI2 来抑制脱落酸(ABA)的反应,而 FER 是生长素促进生长的正调节剂。FER 途径包括与鸟嘌呤核苷酸交换因子 GEF1、GEF4 和 GEF10 相互作用的 FER 激酶,它们依次激活 GTPase ROP11/ARAC10。拟南芥中任何一步 FER 途径的突变体,包括 fer、gef1gef4gef10 或 rop11/arac10,均表现出 ABA 超敏反应,这表明 FER 途径参与了抑制机制。在寻找 FER 途径的靶标时,我们发现 ROP11/ARAC10 蛋白与 ABI2 磷酸酶相互作用并增强其活性,从而将 FER 途径与 ABA 信号的抑制联系起来。