质膜相关的胞质激酶BIK1磷酸化修饰Ca2+泵介导植物避盐性的机制研究

盐胁迫是影响作物产量的重要限制因素。植物盐胁迫响应可分为耐盐与避盐响应，其中避盐响应减轻胁迫伤害。盐胁迫触发钙离子信号，激活SOS信号途径，介导细胞质Na+外排和耐盐性。虽然钙离子信号介导耐盐性的分子机制已被解析，然而其在避盐响应中的作用并不清楚。本研究中，申请人发现植物根部避盐响应依赖钙离子信号；还发现质膜相关的胞质激酶BIK1，以及钙离子泵ACA8和ACA10介导植物根部避盐响应；进一步研究发现BIK1磷酸化修饰ACA8和ACA10自抑制区第57和63位的丝苏氨酸，暗示BIK1可能通过磷酸化ACA8和ACA10发挥功能。在此基础上，申请人将进一步研究盐胁迫下ACA8和ACA10的磷酸化修饰对其功能的调控。本项目的实施将揭示BIK1磷酸化修饰钙离子泵ACA8和ACA10调控植物根部避盐响应的分子机制。该机制的阐明将解析避盐响应中部分早期信号，拓宽我们对盐胁迫下钙离子信号的认知。

Salt stress is the primary environmental factor affecting crop growth and yield. Salt stress responses can be separated into salt tolerance responses and salt avoidance responses. Root halotropism plays a vital role in reducing the damage caused by salt stress. Salt stress triggers Ca2+ signal, which activates the SOS signal pathway and mediates excess Na+ ions out of cells. However, whether and how the Ca2+ signal mediates root halotropism is still unclear. In this study, we found that the root halotropic response depends on Ca2+ signal. The plasma membrane-associated cytoplasmic protein kinase BIK1 and plasma membrane-localized calcium pumps ACA8 and ACA10 control root halotropism. Further study showed that BIK1 could phosphorylate the N-terminal cytoplasmic autoinhibitory fragments of ACA8 and ACA10 at two sites: Ser57 and Thr63. These results suggested that BIK1 may regulate root halotropism through phosphorylation of ACA8 and ACA10. We will further investigate the regulation of ACA8 and ACA10’s function by phosphorylation. Our study is expected to reveal the molecular mechanism that BIK1 phosphorylates ACA8 and ACA10 to regulate root halotropism. This mechanism’s elucidation will uncover part of the early salt stress signaling and broaden our understanding of Ca2+ signaling under salt stress conditions.