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The requirement for yeast superoxide dismutase is bypassed through mutations in BSD2, a novel metal homeostasis gene.

机译:通过新型金属稳态基因BSD2中的突变绕过了酵母超氧化物歧化酶的需求。

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Oxygen toxicity in Saccharomyces cerevisiae strains lacking superoxide dismutase can be suppressed through mutations in either the BSD1 or BSD2 gene. In this report, we demonstrate that the BSD2 gene normally functions in the homeostasis of heavy metal ions. A mutation in BSD2 not only reverses the aerobic defects of yeast strains lacking superoxide dismutase but also is associated with an increased sensitivity to copper and cadmium toxicity and an elevation in copper ion accumulation. The BSD2 gene was cloned by functional complementation and is predicted to encode a novel 37.5-kDa protein with three potential transmembrane domains. The mutant bsd2-1 allele was isolated and found to contain a single C-to-T transition changing a centrally located proline to a serine. This substitution results in total inactivation of BSD2, since the bsd2-1 mutation is identical to a bsd2 delta gene deletion in phenotype. BSD2 is expressed in yeast cells as a 1.5-kb mRNA. Although the gene functions in copper detoxification, BSD2 is not induced by copper ions, as is the case with S. cerevisiae metallothioneins. A probable role for copper ions in the bsd2 reversal of oxidative damage is discussed.
机译:缺乏超氧化物歧化酶的酿酒酵母菌株中的氧中毒可通过BSD1或BSD2基因的突变来抑制。在此报告中,我们证明BSD2基因在重金属离子的体内平衡中正常起作用。 BSD2中的突变不仅可以逆转缺乏超氧化物歧化酶的酵母菌株的需氧缺陷,而且还可以提高对铜和镉毒性的敏感性,并增加铜离子的积累。通过功能互补克隆了BSD2基因,并预测其编码具有三个潜在跨膜结构域的新型37.5-kDa蛋白。分离了突变体bsd2-1等位基因,发现其包含一个单一的从C到T的转变,从而将脯氨酸转变为丝氨酸。这种取代导致BSD2完全失活,因为bsd2-1突变与表型中的bsd2 delta基因缺失相同。 BSD2在酵母细胞中以1.5-kb mRNA的形式表达。尽管该基因在铜排毒中起作用,但BSD2不受铜离子诱导,就像酿酒酵母金属硫蛋白一样。讨论了铜离子在bsd2逆转氧化损伤中的可能作用。

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