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.

植物作为固着生物，必须适应环境的变化。环境胁迫触发各种反应，包括植物激素脱落酸（ABA）介导的生长抑制。人们对将压力反应与增长相结合的机制了解甚少。在这里，我们发现雷帕霉素（TOR）激酶的靶标在保守的丝氨酸残基上磷酸化PYL ABA受体，以防止未胁迫植物中应激反应的激活。这种磷酸化破坏了PYL与ABA和PP2C磷酸酶效应子的缔合，导致SnRK2激酶失活。在压力下，ABA激活的SnRK2s磷酸化Raptor（TOR复合物的一个组成部分），触发TOR复合物的解离和抑制。因此，TOR信号在非胁迫条件下会抑制ABA信号和应激反应，而ABA信号转导在压力时期抑制TOR信号转导和生长。植物利用这种保守的磷调节反馈机制来优化生长和胁迫响应的平衡。