Instituto Gulbenkian de Ciência, GREEN-IT Bioresources for Sustainability, Oeiras, Portugal.
Instituto de Biología Molecular y Celular de Plantas, Consejo Superior de Investigaciones Científicas-Universidad Politécnica de Valencia, Valencia, Spain.
Nat Plants. 2020 Nov;6(11):1345-1353. doi: 10.1038/s41477-020-00778-w. Epub 2020 Oct 19.
Adverse environmental conditions trigger responses in plants that promote stress tolerance and survival at the expense of growth. 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.
不利的环境条件会引发植物的应激反应，以牺牲生长为代价来提高其对压力的耐受性和生存能力。然而，人们对于应激信号通路如何相互作用以及与生长调节成分相互作用以平衡生长和应激反应知之甚少。在这里，我们表明植物的生长在很大程度上受到进化保守的能量感应 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，但我们揭示了这些激酶在没有 ABA 的情况下出人意料的促进生长的功能，它们作为 SnRK1 的抑制剂来抑制 SnRK1 信号。SnRK2 包含的复合物对 SnRK1 的隔离抑制了 SnRK1 信号，从而允许雷帕霉素靶蛋白（TOR）在最佳条件下发挥活性和生长。另一方面，这些复合物对于 ABA 响应中 SnRK1 的释放和激活是必不可少的，从而导致 TOR 的抑制和应激下的生长。SnRK2 激酶对 SnRK1 的这种双重调节将生长控制与陆地生境特有的环境因素联系起来，这对于植物从水生到陆生的过渡可能是至关重要的。
