Shanghai Center for Plant Stress Biology, CAS Center of Excellence in Molecular Plant Sciences, Chinese Academy of Sciences, Shanghai 200032, China; Department of Horticulture and Landscape Architecture, Purdue University, West Lafayette, IN 47907, USA.
Shanghai Center for Plant Stress Biology, CAS Center of Excellence in Molecular Plant Sciences, Chinese Academy of Sciences, Shanghai 200032, China.
Mol Cell. 2018 Jan 4;69(1):100-112.e6. doi: 10.1016/j.molcel.2017.12.002. Epub 2017 Dec 28.
As sessile organisms, plants must adapt to variations in the environment. Environmental stress triggers various responses, including growth inhibition, mediated by the plant hormone abscisic acid (ABA). The mechanisms that integrate stress responses with growth are poorly understood. Here, we discovered that the Target of Rapamycin (TOR) kinase phosphorylates PYL ABA receptors at a conserved serine residue to prevent activation of the stress response in unstressed plants. This phosphorylation disrupts PYL association with ABA and with PP2C phosphatase effectors, leading to inactivation of SnRK2 kinases. Under stress, ABA-activated SnRK2s phosphorylate Raptor, a component of the TOR complex, triggering TOR complex dissociation and inhibition. Thus, TOR signaling represses ABA signaling and stress responses in unstressed conditions, whereas ABA signaling represses TOR signaling and growth during times of stress. Plants utilize this conserved phospho-regulatory feedback mechanism to optimize the balance of growth and stress responses.
作为固着生物,植物必须适应环境变化。环境胁迫引发各种反应,包括生长抑制,这是由植物激素脱落酸(ABA)介导的。将应激反应与生长整合的机制还知之甚少。在这里,我们发现雷帕霉素靶蛋白(TOR)激酶在保守丝氨酸残基上磷酸化 PYL ABA 受体,以防止未受应激植物的应激反应激活。这种磷酸化会破坏 PYL 与 ABA 和 PP2C 磷酸酶效应物的结合,导致 SnRK2 激酶失活。在应激下,ABA 激活的 SnRK2 磷酸化 Raptor,这是 TOR 复合物的一个组成部分,触发 TOR 复合物解离和抑制。因此,TOR 信号在未受应激条件下抑制 ABA 信号和应激反应,而 ABA 信号在应激时抑制 TOR 信号和生长。植物利用这种保守的磷酸化调节反馈机制来优化生长和应激反应之间的平衡。