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在重金属毒性下,UGA4和YBR062C调节氧化应激耐受性

Mustafa Al-Gafari^1,2,3, Houman Moteshareie^1,2,3, Thomas D D Kazmirchuk^1,2,3

¹Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|March 9, 2026

概括

两个新的基因UGA4和YBR062C通过改善Ure2p蛋白的内部核糖体进入部位 (IRES) 介导翻译来增强酵母对等重金属的耐药性.

科学领域:

细胞应激反应的细胞应激反应
基因调节基因调节
金属毒性金属毒性

背景情况:

重金属通过氧化损伤和蛋白质功能障碍诱导细胞应激.
Ure2p是Saccharomyces cerevisiae中的一种谷氨S转移酶,它能抵抗金属诱导的氧化应激.
尿素2p的合成是由URE2 5' UTR中应激反应的内部核糖体进入部位 (IRES) 调节的.

研究的目的:

调查重金属应激反应中基因调节的机制细节.
确定Saccharomyces cerevisiae中对重金属耐受性的新贡献者.
阐明UGA4和YBR062C在金属电阻路径中的作用.

主要方法:

在Saccharomyces cerevisiae中进行基因缺失和过度表达研究.
使用殖民地形成单元测试评估金属灵敏度.
基因分析,包括双重突变结构.
在压力条件下分析URE2mRNA和URE2p蛋白水平.
多元体概况以评估翻译效率.
使用URE2-IRES-依赖的报告测试.

主要成果:

UGA4和YBR062C的删除突变对,矿和具有显著的敏感性.
UGA4 和 YBR062C 在 URE2 途径中起作用,而双重突变体与单一的 ure2Δ 突变体相比没有增加的敏感性.
在uga4Δ和ybr062cΔ突变体中,URE2的过度表达挽救了金属电阻.
UGA4和YBR062C在转录后起作用,降低Ure2p蛋白水平而不会影响URE2 mRNA丰度.
在突变者中观察到URE2mRNA的核糖体关联减少和IRES依赖的记者活性减少.
卡普依赖转化和记者mRNA水平没有受到影响.

结论:

UGA4和YBR062C是Saccharomyces cerevisiae中重金属耐受性的新型贡献者.
这些基因通过增强URE2mRNA的IRES介导翻译来促进重金属耐药性.
这些发现揭示了压力反应基因的新调节机制,涉及IRES元素和辅助因素.

关键词:

这里是IRES IRES.在此之前,URE2 重金属重金属的使用.氧化应激是一种氧化应激.翻译翻译翻译翻译翻译翻译酵母酵母是一种酵母.

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