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

C2H2-type zinc finger transcription factor sensitive to proton rhizotoxicity 1 (STOP1) plays an essential role in aluminium (Al) resistance inArabidopsis thalianaby controlling the expression of a set of Al-resistance genes, including the malate transporter-encoding geneA. thaliana aluminium activated malate transporter 1(AtALMT1) that is critically required for Al resistance.STOP1is suggested to be modulated by Al at post-transcriptional and/or post-translational levels. However, the underlying molecular mechanisms remain to be demonstrated. We carried out a forward genetic screen on an ethyl methanesulphonate mutagenized population, which contains theAtALMT1promoter-driven luciferase reporter gene (pAtALMT1:LUC), and identifiedhyperrecombination protein 1(HPR1), which encodes a subunit of the THO/TREX complex. We investigate the effect ofhpr1mutations on the expression of Al-resistance genes and Al resistance, and we also examined the regulatory role of HPR1 in nuclear messenger RNA (mRNA) and protein accumulation ofSTOP1gene. Mutation ofHPR1reduces the expression of STOP1-regulated genes and the associated Al resistance. Thehpr1mutations increaseSTOP1mRNA retention in the nucleus and consequently decrease STOP1 protein abundance. Mutation ofregulation of AtALMT1 expression 1(RAE1) that mediates STOP1 degradation in thehpr1mutant background can partially rescue the deficient phenotypes ofhpr1mutants. Our results demonstrate that HPR1 modulates Al resistance partly through the regulation of nucleocytoplasmicSTOP1mRNA export.