Mg²⁺ is among the most abundant divalent cations in living cells. In plants, investigations on magnesium (Mg) homeostasis are restricted to the functional characterization of Mg²⁺ transporters. Here, we demonstrate that the splicing factors SUPPRESSORS OF MEC-8 AND UNC-52 1 (SMU1) and SMU2 mediate Mg homeostasis in Arabidopsis (Arabidopsis thaliana). A low-Mg sensitive Arabidopsis mutant was isolated, and the causal gene was identified as SMU1. Disruption of SMU2, a protein that can form a complex with SMU1, resulted in a similar low-Mg sensitive phenotype. In both mutants, an Mg²⁺ transporter gene, Mitochondrial RNA Splicing 2 (MRS2-7), showed altered splicing patterns. Genetic evidence indicated that MRS2-7 functions in the same pathway as SMU1 and SMU2 for low-Mg adaptation. In contrast with previous results showing that the SMU1-SMU2 complex is the active form in RNA splicing, MRS2-7 splicing was promoted in the smu2 mutant overexpressing SMU1, indicating that complex formation is not a prerequisite for the splicing. We found here that formation of the SMU1-SMU2 complex is an essential step for their compartmentation in the nuclear speckles, a type of nuclear body enriched with proteins that participate in various aspects of RNA metabolism. Taken together, our study reveals the involvement of the SMU splicing factors in plant Mg homeostasis and provides evidence that complex formation is required for their intranuclear compartmentation.

Mg ²⁺是活细胞中最丰富的二价阳离子之一。在植物中，对镁 (Mg) 稳态的研究仅限于 Mg ²⁺转运蛋白的功能表征。在这里，我们证明了MEC-8 和 UNC-52 1 ( SMU1 ) 和SMU2的剪接因子抑制剂介导拟南芥 ( Arabidopsis thaliana ) 中的镁稳态。分离出低镁敏感拟南芥突变体，并将其致病基因鉴定为SMU1 。 SMU2（一种可以与 SMU1 形成复合物的蛋白质）的破坏导致了类似的低镁敏感表型。在这两种突变体中，Mg ²⁺转运蛋白基因线粒体 RNA 剪接 2 ( MRS2-7 ) 显示出剪接模式的改变。遗传证据表明， MRS2-7 的功能与SMU1和SMU2具有相同的低镁适应途径。与先前显示SMU1-SMU2复合物是RNA剪接中的活性形式的结果相反， MRS2-7剪接在过表达SMU1的smu2突变体中得到促进，表明复合物形成不是剪接的先决条件。我们在这里发现，SMU1-SMU2 复合物的形成是它们在核斑点中划分的重要步骤，核斑点是一种富含参与 RNA 代谢各个方面的蛋白质的核体。综上所述，我们的研究揭示了 SMU 剪接因子在植物镁稳态中的参与，并提供了其核内区室需要复杂形成的证据。