Abstract

Boric acid is essential for plants and has many vital roles in animals and microorganisms. However, its high doses are toxic to all organisms. We previously screened yeast deletion collections to identify boric acid-resistant and susceptible mutants to identify genes that play a role in boron tolerance. Here, we analyzed boron resistant mutants (elp1∆, elp3∆, elp6∆, ncs2∆, ncs6∆ and kti12∆) for their abilities to modulate the general amino acid control system (GAAC) and to induce boron efflux pump ATR1. The mutants analyzed in this study lack the genes that play roles in tRNA Wobble base modifications. We found that all of the boron resistant mutants activated Gcn4-dependent reporter gene activity and increased the transcript level of the ATR1 gene. Additionally, boron resistant cells accumulated less boric acid in their cytoplasm compared to the wild type cells upon boron exposure. Thus, our findings suggested that loss of wobble base modifications in tRNA leads to GAAC activation and ATR1 induction, which in turn reduced intracellular boron levels and caused boron resistance.

中文翻译：

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酵母中的tRNA摆动碱基修饰和硼酸抗性：耐硼缺失突变体诱导一般氨基酸控制机制并激活硼外流。

摘要

硼酸对植物至关重要，在动物和微生物中具有许多重要作用。但是，其高剂量对所有生物都有毒。我们先前筛选了酵母缺失集合，以鉴定抗硼酸和易感突变体，以鉴定在硼耐受性中发挥作用的基因。在这里，我们分析了抗硼突变体（elp1 ∆，elp3 ∆，elp6 ∆，ncs2 ∆，ncs6 ∆和kti12 ∆）调节常规氨基酸控制系统（GAAC）并诱导硼外排泵ATR1的能力。。在这项研究中分析的突变体缺乏在tRNA摆动碱基修饰中起作用的基因。我们发现所有抗硼突变体均激活Gcn4依赖的报告基因活性并增加ATR1基因的转录水平。另外，与硼暴露后的野生型细胞相比，抗硼细胞在其细胞质中积累的硼酸更少。因此，我们的发现表明，tRNA中摆动碱基修饰的丢失会导致GAAC活化和ATR1诱导，进而降低细胞内硼水平并引起硼抗性。