背景回顾：Aluminum (Al) toxicity can seriously restrict crop production on acidic soils, which comprise 40% of the world’s potentially arable land. The zinc finger transcription factor STOP1 has a conserved and essential function in mediating plant Al resistance. Al stress induces STOP1 accumulation via post-transcriptional regulatory mechanisms. 

提出问题：However, the upstream signaling pathway involved in Al-triggered STOP1 accumulation remains unclear. 

主要发现：Here, we report that the MEKK1-MKK1/2-MPK4 cascade positively regulates STOP1 phosphorylation and stability. 

结果1-MEKK1-MKK1/2-MPK4突变：Mutations of MEKK1, MKK1/2, or MPK4 lead to decreased STOP1 stability and Al resistance. 

结果2-MPK4磷酸化STOP1：Al stress induces the kinase activity of MPK4, which interacts with and phosphorylates STOP1. 

结果3-STOP1磷酸化减少蛋白降解：The phosphorylation of STOP1 reduces its interaction with the F-box protein RAE1 that mediates STOP1 degradation, thereby leading to enhanced STOP1 stability and Al resistance. 

结论：Taken together, our results suggest that the MEKK1-MKK1/2-MPK4 cascade is important for Al signaling and confers Al resistance through phosphorylation-mediated enhancement of STOP1 accumulation in Arabidopsis.

铝毒严重限制酸性土壤上的作物产量，而酸性土壤占了全球40%的潜在耕地。锌指转录因子STOP1在介导植物的铝耐受性方面存在重要作用。铝胁迫通过转录后的调控机制诱导STOP1的积累。但是，涉及铝诱导的STOP1积累的上游信号转导通路还不清楚。本文中，作者报道了MEKK1-MKK1/2-MPK4级联正调控STOP1的磷酸化和稳定性。MEKK1，MKK1/2或者MPK4的突变会导致的STOP1稳定性降低，对铝胁迫的抗性也减弱。铝胁迫诱导MPK4的激酶活性，而MPK4与STOP1互作促使后者的磷酸化。STOP1的磷酸化减少了其与F-box蛋白RAE1的互作，从而减少了STOP1蛋白的降解，最终导致STOP1蛋白稳定性和铝胁迫抗性增强。综上，本文的研究结果揭示了MEKK1-MKK1/2-MPK4级联对于植物的铝信号转导非常重要，通过磷酸化介导的STOP1积累增强从而增加拟南芥的铝胁迫抗性。