王存等《Nature communications》2023年

作者: 来源:伟德BETVLCTOR1946 发布日期:2023-09-22 浏览次数:

论文题目:The CBL1/9-CIPK1 calcium sensor negativelyregulates drought stress by phosphorylatingthe PYLs ABA receptor

论文作者:Zhang You, Shiyuan Guo, Qiao Li, Yanjun Fang, Panpan Huang, Chuanfeng Ju & Cun Wang

论文摘要:The stress hormone, Abscisic acid (ABA), is crucial for plants to respond tochanges in their environment. It triggers changes in cytoplasmic Ca2+ levels,which activate plant responses to external stresses. However, how Ca2+ sensingand signaling feeds back into ABA signaling is not well understood. Here wereveal a calcium sensing module that negatively regulates drought stress viamodulating ABA receptor PYLs. Mutants cbl1/9 and cipk1 exhibit hypersensitivityto ABA and drought resilience. Furthermore, CIPK1 is shown to interactwith and phosphorylate 7 of 14 ABA receptors at the evolutionarily conservedsite corresponding to PYL4 Ser129, thereby suppressing their activities andpromoting PP2C activities under normal conditions. Under drought stress,ABA impedes PYLs phosphorylation by CIPK1 to respond to ABA signaling andsurvive in unfavorable environment. These findings provide insights into apreviously unknown negative regulatory mechanism of the ABA signalingpathway, which is mediated by CBL1/9-CIPK1-PYLs, resulting in plants that aremore sensitive to drought stress. This discovery expands our knowledge aboutthe interplay between Ca2+ signaling and ABA signaling.

逆境激素脱落酸(ABA)对植物应对环境变化至关重要。它引发细胞质Ca2+水平的变化,从而激活植物对外部胁迫的响应。然而,目前对Ca2+的感知和信号传导如何反馈到ABA信号中还不是很清楚。我们描绘了一个钙传感模块,它通过调节ABA受体PYLs负向调节干旱胁迫。拟南芥cbl1/9和cipk1突变体显示出对ABA超敏和干旱耐受。进一步的研究发现CIPK1与14个ABA受体中的7个相互作用,并在与对应于PYL4 Ser129的进化保守位点上磷酸化ABA受体,从而在正常条件下抑制其活性并促进PP2C的活性。在干旱胁迫下,ABA会阻碍PYLs被CIPK1磷酸化,以响应ABA信号,确保植物在不利环境中生存。这些发现让我们深入了解了之前未知的ABA信号通路负调控机制,该机制由CBL1/9-CIPK1-PYLs功能模块介导,导致植物对干旱胁迫更加敏感。这一发现拓展了我们对Ca2+信号传导与ABA信号传导之间相互作用的认识。

论文链接:https://doi.org/10.1038/s41467-023-41657-0