Yeast lacking superoxide dismutase. Isolation of genetic suppressors.

Yeast lacking superoxide dismutase. Isolation of genetic suppressors.
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DOI:
10.1016/s0021-9258(19)36959-5
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发表时间:
1992-09
期刊:
The Journal of biological chemistry
影响因子:
--
通讯作者:
X. Liu;I. Elashvili;E. B. Gralla;J. Valentine;P. Lapinskas;V. Culotta
X. Liu;I. Elashvili;E. B. Gralla;J. Valentine;P. Lapinskas;V. Culotta
中科院分区:
其他
文献类型:
--
作者:
X. Liu;I. Elashvili;E. B. Gralla;J. Valentine;P. Lapinskas;V. Culotta

文献摘要

被引文献

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酿酒酵母超氧化物歧化酶(SOD)的突变体与许多生化缺陷相关。除了对氧毒性高度敏感之外,在SOD 1(编码Cu/Zn-SOD)和SOD 2(编码Mn-SOD)基因中都含有缺失的菌株在孢子形成中有缺陷,与高突变率相关,并且不能生物合成赖氨酸和甲硫氨酸。详细探讨了赖氨酸代谢中的SOD相关缺陷,发现其发生在赖氨酸生物合成的早期步骤,显然是在α-氨基己二酸转氨酶水平。为了更好地理解SOD在细胞代谢中的作用,我们的实验室分离了绕过SOD缺陷的酵母抑制子(“bsd”菌株),即S。酿酒酵母细胞缺乏SOD,但耐氧毒性。两个核bsd互补组已被确定,都抑制了各种生物缺陷与sod 1和sod 2无效突变体。这些结果表明,单个基因突变可以减轻细胞生长对SOD的需求。两个bsd互补组都不能利用许多不可发酵的碳源,这表明在电子传递中可能存在抑制子相关的缺陷。
Null mutants of superoxide dismutase (SOD) in Saccharomyces cerevisiae are associated with a number of biochemical defects. In addition to being hypersensitive to oxygen toxicity, strains containing deletions in both the SOD1 (encoding Cu/Zn-SOD) and SOD2 (encoding Mn-SOD) genes are defective in sporulation, are associated with a high mutation rate, and are unable to biosynthesize lysine and methionine. The sod-linked defect in lysine metabolism was explored in detail and was found to occur at an early step in lysine biosynthesis, evidently at the level of the alpha-amino adipate transaminase. To better understand the role of SOD in cell metabolism, our laboratory has isolated yeast suppressors that have bypassed the SOD defect (“bsd” strains), that is, S. cerevisiae cells lacking SOD, yet resistant to oxygen toxicity. Two nuclear bsd complementation groups have been identified, and both suppress a variety of biological defects associated with sod1 and sod2 null mutants. These results demonstrate that a single gene mutation can alleviate the requirement for SOD in cell growth. Both bsd complementation groups are unable to utilize many non-fermentable carbon sources, suggesting a possible suppressor-linked defect in electron transport.