Mutation of HPR1 encoding a component of the THO/TREX complex reduces STOP1 accumulation and aluminum resistance in Arabidopsis thaliana.

C2H2-type zinc finger transcription factor STOP1 plays an essential role in aluminum (Al) resistance in Arabidopsis thaliana by controlling the expression of a set of Al-resistance genes including the malate transporter-encoding gene AtALMT1 that is critically required for Al resistance. STOP1 is suggested to be modulated by Al at posttranscriptional and/or posttranslational levels. However, the underlying molecular mechanisms remain to be demonstrated. We carried out a forward genetic screen on an EMS-mutagenized population, which contains the AtALMT1 promoter-driven luciferase reporter gene (pAtALMT1:LUC), and identified HPR1, which encodes a subunit of the THO/TREX complex. We investigate the effect of hpr1 mutations on the expression of Al-resistance genes and Al resistance, and we also examined the regulatory role of HPR1 in nuclear mRNA and protein accumulation of STOP1 gene. Mutation of HPR1 reduces the expression of STOP1-regulated genes and the associated Al resistance. The hpr1 mutations increase STOP1 mRNA retention in the nucleus and consequently decrease STOP1 protein abundance. Mutation of RAE1 that mediates STOP1 degradation in the hpr1 mutant background can partially rescue the deficient phenotypes of hpr1 mutants. Our results demonstrate that HPR1 modulates Al resistance partly through the regulation of nucleocytoplasmic STOP1 mRNA export.