AhASRK1, a peanut dual-specificity kinase that activates the Ca-ROS-MAPK signalling cascade to mediate programmed cell death induced by aluminium toxicity via ABA.

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.