Adverse environmental conditions trigger responses in plants that promote stress tolerance and survival at the expense of growth¹. However, little is known of how stress signalling pathways interact with each other and with growth regulatory components to balance growth and stress responses. Here, we show that plant growth is largely regulated by the interplay between the evolutionarily conserved energy-sensing SNF1-related protein kinase 1 (SnRK1) protein kinase and the abscisic acid (ABA) phytohormone pathway. While SnRK2 kinases are main drivers of ABA-triggered stress responses, we uncover an unexpected growth-promoting function of these kinases in the absence of ABA as repressors of SnRK1. Sequestration of SnRK1 by SnRK2-containing complexes inhibits SnRK1 signalling, thereby allowing target of rapamycin (TOR) activity and growth under optimal conditions. On the other hand, these complexes are essential for releasing and activating SnRK1 in response to ABA, leading to the inhibition of TOR and growth under stress. This dual regulation of SnRK1 by SnRK2 kinases couples growth control with environmental factors typical for the terrestrial habitat and is likely to have been critical for the water-to-land transition of plants.

不利的环境条件会触发植物的反应，以牺牲生长为代价来促进胁迫耐受性和存活¹. 然而，人们对压力信号通路如何相互作用以及如何与生长调节成分相互作用以平衡生长和压力反应知之甚少。在这里，我们表明植物生长在很大程度上受进化上保守的能量感应 SNF1 相关蛋白激酶 1 (SnRK1) 蛋白激酶和脱落酸 (ABA) 植物激素途径之间的相互作用的调节。虽然 SnRK2 激酶是 ABA 触发的应激反应的主要驱动因素，但我们发现了在没有 ABA 作为 SnRK1 阻遏物的情况下这些激酶的意外生长促进功能。含有 SnRK2 的复合物对 SnRK1 的隔离会抑制 SnRK1 信号传导，从而允许雷帕霉素 (TOR) 活性和在最佳条件下生长的目标。另一方面，这些复合物对于响应 ABA 释放和激活 SnRK1 是必不可少的，导致压力下的 TOR 和生长受到抑制。SnRK2 激酶对 SnRK1 的这种双重调节将生长控制与陆地栖息地的典型环境因素结合起来，并且可能对植物的水陆过渡至关重要。