Li Kun-Lun, Xue Hui, Tang Ren-Jie, Luan Sheng
Department of Plant and Microbial Biology, University of California, Berkeley, CA 94720, USA.
Institute of Future Agriculture, Northwest A&F University, Yangling, Shaanxi 712100, China.
Plant Cell. 2025 Jul 1;37(7). doi: 10.1093/plcell/koaf103.
Soil salinity negatively affects crop yields worldwide. The dynamic transition between growth and salt stress responses helps plants cope with changing soil salinity status. However, the molecular mechanisms controlling such dynamic transitions remain poorly understood. Here, our study identified the target of rapamycin complex (TORC) as a central player in growth recovery from salt stress. We observed a rapid decline in TORC activity in Arabidopsis thaliana plants upon exposure to salt stress. Further investigation uncovered an intricate interplay between TORC and a salt response signaling network comprising calcineurin B-like (CBL) proteins and CBL-interacting kinases (CIPKs). Under standard growth conditions, Regulatory-Associated Protein of TOR (RAPTOR) promotes CBL-CIPK complex dissociation, thereby inhibiting CIPK. CIPK suppression is lifted under salt stress, and the activated CBL-CIPK complex phosphorylates RAPTOR, which in turn suppresses TORC activity. Thus, the reciprocal regulation of the TORC and CBL-CIPK modules orchestrates plant responses and adaptation to soil salinity.
土壤盐度对全球作物产量产生负面影响。生长与盐胁迫响应之间的动态转变有助于植物应对不断变化的土壤盐度状况。然而,控制这种动态转变的分子机制仍知之甚少。在此,我们的研究确定雷帕霉素靶蛋白复合体(TORC)是植物从盐胁迫中恢复生长的核心调控因子。我们观察到拟南芥植株在受到盐胁迫时,TORC活性迅速下降。进一步研究发现,TORC与一个由类钙调磷酸酶B蛋白(CBL)和CBL互作激酶(CIPK)组成的盐胁迫响应信号网络之间存在复杂的相互作用。在标准生长条件下,TOR调节相关蛋白(RAPTOR)促进CBL-CIPK复合体解离,从而抑制CIPK。在盐胁迫下,CIPK的抑制作用解除,被激活的CBL-CIPK复合体使RAPTOR磷酸化,进而抑制TORC活性。因此,TORC和CBL-CIPK模块之间的相互调控协调了植物对土壤盐度的响应和适应。