Fu Xue-Zhen, Wang Xin, Liu Jing-Jing, Chen Yu-Xi, Wang Ai-Qin, Zhan Jie, Han Zhu-Qiang, He Long-Fei, Xiao Dong
Guangxi Key Laboratory for Agro-Environment and Agro-Product Safety, College of Agriculture, GuangXi University, Nanning, 530004, China; National Demonstration Center for Experimental Plant Science Education/College of Agriculture, Nanning, 530004, China; Guangxi University Key Laboratory of Crop Cultivation and Tillage, Nanning, 530004, China.
Cash Crops Research Institute, Guangxi Academy of Agricultural Science, Nanning, 530007, China.
Plant Physiol Biochem. 2025 Mar;220:109538. doi: 10.1016/j.plaphy.2025.109538. Epub 2025 Jan 21.
Aluminium (Al)-induced programmed cell death (PCD) is thought to be a main cause of Al phytotoxicity. However, the underlying mechanism by which Al induces PCD in plants is unclear. In this study, we characterized the function of AhASRK1 (Aluminum Sensitive Receptor-like protein Kinase1), an Al-induced LRR-type receptor-like kinase gene. AhASRK1 was localized on the plasma membrane. A kinase assay of recombinant cytoplasmic domains of AhASRK1 revealed that this leucine-rich repeat-receptor-like protein kinase autophosphorylates both serine/threonine and tyrosine residues. The role of AhASRK1 in regulating Al-induced PCD was investigated in roots. Al treatment significantly inhibited root growth and promoted ROS production and cell death after AhASRK1 was overexpressed in Arabidopsis, whereas the knockdown of AhASRK1 in peanut increased Al tolerance. AhASRK1 overexpression resulted in increased accumulation of apical calcium ions (Ca) and increased MAPK signalling under Al treatment; however, the AhASRK1-knockdown peanut lines exhibited a decrease in the Ca concentration under Al stress. Furthermore, inhibition of ABA biosynthesis mitigated PCD occurrence and ROS accumulation under Al stress, as did Al-induced Ca and p MAPK signalling. These results suggest that AhASRK1 mediates the occurrence of PCD through the ABA pathway to mediate the accumulation of Ca and the production of ROS, thereby activating MAPK signalling. Additionally, AhASRK1 overexpression promoted leaf senescence and induced the transcription of a multitude of ABA-related genes. This study provides new clues for improving the phytotoxicity of Al in acidic soils.
铝（Al）诱导的程序性细胞死亡（PCD）被认为是铝对植物产生毒害作用的主要原因。然而，铝在植物中诱导PCD的潜在机制尚不清楚。在本研究中，我们对AhASRK1（铝敏感类受体蛋白激酶1）的功能进行了表征，AhASRK1是一个受铝诱导的富含亮氨酸重复序列（LRR）的类受体激酶基因。AhASRK1定位于质膜上。对AhASRK1重组胞质结构域进行激酶活性分析发现，这种富含亮氨酸重复序列的类受体蛋白激酶能使丝氨酸/苏氨酸和酪氨酸残基发生自磷酸化。我们在根中研究了AhASRK1在调节铝诱导的PCD中的作用。在拟南芥中过表达AhASRK1后，铝处理显著抑制了根的生长，并促进了活性氧（ROS）的产生和细胞死亡，而在花生中敲低AhASRK1则提高了对铝的耐受性。过表达AhASRK1导致在铝处理下顶端钙离子（Ca）积累增加以及促分裂原活化蛋白激酶（MAPK）信号增强；然而，敲低AhASRK1的花生品系在铝胁迫下Ca浓度降低。此外，抑制脱落酸（ABA）生物合成减轻了铝胁迫下PCD的发生和ROS的积累，铝诱导的Ca和磷酸化MAPK信号也有同样的效果。这些结果表明，AhASRK1通过ABA途径介导PCD的发生，以介导Ca的积累和ROS的产生，从而激活MAPK信号。此外，AhASRK1过表达促进了叶片衰老，并诱导了大量与ABA相关基因的转录。本研究为改善酸性土壤中铝对植物的毒害作用提供了新线索。
