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Aluminum (Al) toxicity can seriously restrict crop production in acidic soils, which comprise 40% of the world's potentially arable land. The zinc finger transcription factor STOP1 has a conserved and essential function mediating plant Al resistance. Aluminum stress induces STOP1 accumulation via post-transcriptional regulatory mechanisms. However, the upstream signaling pathway involved in Al-triggered STOP1 accumulation remains unclear. We herein report that the MEKK1-MKK1/2-MPK4 cascade positively regulates STOP1 phosphorylation and stability. Mutations of MEKK1, MKK1/2 or MPK4 lead to decreased STOP1 stability and Al resistance. Additionally, Al stress induces the kinase activity of MPK4, which interacts with and phosphorylates STOP1. 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. Taken together, our results suggest that the MEKK1-MKK1/2-MPK4 cascade is important for Al signaling and conferring Al resistance by phosphorylation-mediated enhancement of STOP1 accumulation in Arabidopsis. |
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