拟南芥钙依赖蛋白激酶CPK21和CPK23调控植物耐铝性的生理及分子机理

铝（Al）毒害是酸性土壤上限制作物生产的主要因子之一。明确植物耐铝性分子调控机制，发掘植物耐铝调控关键基因，是利用现代生物手段改良植物营养遗传性状，最终培育适应酸性铝毒土壤植物新品种的前提。我们前期研究发现铝胁迫下CPK21和CPK23通过影响ALMT1和MATE介导的根系有机酸的分泌进而调控植物耐铝性。本项目拟在前期研究的基础上，结合生理生化、细胞学、遗传学及分子生物学等技术和手段，继续深入探讨铝胁迫下CPK21和CPK23调控植物耐铝性的生理和分子机理，阐明铝胁迫下CPK21和CPK23如何通过作用于STOP1进而调控ALMT1和MATE表达的分子机理，明确CPK21和CPK23对植物耐铝性的调控是否依赖于Ca2+信号，筛选CPK21和CPK23蛋白关键调控或修饰因子，并明确其在植物耐铝性中的生理和分子作用机理。为最终阐明CPK21和CPK23调控植物耐铝性的生理和分子机理提供依据。

Aluminum (Al) toxicity is one of the major limiting factors for crop production in acid soil. Understanding of the physiological and molecular resistance mechism of plants to Al stress is the prerequirement for the improvement of yield in the breeding for adaptaion to Al toxicity in acid soil. We previously found that CPK21 and CPK23 was involved in the regulation of Al resistance through mediating ALMT1 and MATE-dependent malate and citrate exudation from roots. To further better understand the molecular regulatory mechanism of CPK21 and CPK23 in Al resistance, the physiological, biochemical, cellular, genetic and molecular approaches will be combined in the present study, and will (i): clarify how CPK21 and CPK23 regualtes ALMT1and MATE expression through interaction with STOP1, a key transcription factor in the regulation of Al resistance; (ii) clarify if the CPK-STOP1-ALMT1/MATE regulatory process is Ca2+-dependent or not; (iii) obtain the key CPK21- and CPK23-interacting transcription factors or regulatory proteins , and clarify their molecular and physiological functions in the regulation of Al resistance.