The molecular mechanism of aluminum toxicity in biological systems is not completely understood. Saccharomyces cerevisiae is one of the most used model organisms in the study of environmental metal toxicity. Using an unbiased metallomic approach in yeast, we found that aluminum treatment caused phosphorus deprivation, and the lack of phosphorus increased as the pH of the environment decreased compared to the control strain. By screening the PHO pathway in yeast with the synthetic lethality of a new phosphorus-restricted aluminum-sensitive gene, we observed that pho84Δ mutation conferred severe growth defect to aluminum under low-phosphorus conditions, and the addition of phosphate alleviated this sensitivity. Subsequently, the data showed that PHO84 determined the intracellular aluminum-induced phosphorus deficiency, and the expression of PHO84 was positively correlated with aluminum stress, which was mediated by phosphorus through the coordinated regulation of PHO4/PHO2. Moreover, aluminum reduced phosphorus absorption and inhibited tobacco plant growth in acidic media. In addition, the high-affinity phosphate transporter NtPT1 in tobacco exhibited similar effects to PHO84, and overexpression of NtPT1 conferred aluminum resistance in yeast cells. Taken together, positive feedback regulation of the PHO pathway centered on the high-affinity phosphate transporters is a highly conservative mechanism in response to aluminum toxicity. The results may provide a basis for aluminum-resistant microorganisms or plant engineering and acidic soil treatment.

中文翻译：

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转运蛋白 PHO84/NtPT1 是铝影响酿酒酵母和烟草中磷吸收的靶标。

生物系统中铝毒性的分子机制尚不完全清楚。酿酒酵母是环境金属毒性研究中最常用的模型生物之一。在酵母中使用无偏金属组学方法，我们发现铝处理会导致磷缺乏，并且与对照菌株相比，随着环境 pH 值的降低，磷的缺乏会增加。通过用新的磷限制性铝敏感基因的合成致死率筛选酵母中的PHO途径，我们观察到pho84Δ突变导致低磷条件下铝严重生长缺陷，而磷酸盐的添加缓解了这种敏感性。随后数据显示，PHO84决定了细胞内铝诱导的磷缺乏，且PHO84的表达与铝胁迫呈正相关，而铝胁迫是由磷通过PHO4/PHO2的协调调节来介导的。此外，铝减少了磷的吸收并抑制了酸性介质中烟草植物的生长。此外，烟草中的高亲和力磷酸转运蛋白NtPT1表现出与PHO84相似的作用，并且NtPT1的过度表达赋予酵母细胞铝抗性。总而言之，以高亲和力磷酸盐转运蛋白为中心的 PHO 途径的正反馈调节是响应铝毒性的高度保守机制。研究结果可为抗铝微生物或植物工程和酸性土壤处理提供依据。