A novel ethanol-hypersensitive mutant of Arabidopsis
A novel ethanol-hypersensitive mutant of Arabidopsis
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DOI：
10.1093/pcp/pch078
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发表时间：
2004-06-01
影响因子：
4.9
通讯作者：
Shinozaki, K
中科院分区：
文献类型：
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作者：
Hirayama, T;Fujishige, N;Shinozaki, K
从拟南芥（Arabidopsis thaliana）中分离到一个新的乙醇过敏突变体geko 1（gek 1）。gek 1突变体显示出对生长培养基中乙醇的敏感性增强（比野生型高10-100倍），而它在没有乙醇的情况下正常生长，并对其他醇类和环境胁迫（如热休克和高盐度）正常响应。gek 1的乙醇过敏表型需要乙醇脱氢酶活性，表明gek 1是敏感的，而不是乙醇本身，但乙醇的代谢产物。与此一致，gek 1显示出对培养基中乙醛的增强的敏感性。乙醇处理的gek 1 -2和野生型幼苗的内源乙醛水平没有差异。这些结果表明，乙醇过敏的gek 1是由于增强的敏感性，乙醛毒性，而不是异常升高的积累毒性乙醛，这已被认为是在哺乳动物细胞中的乙醇毒性的主要原因。
A novel ethanol-hypersensitive mutant, geko1 (gek1), was isolated from Arabidopsis thaliana. The gek1 mutant displays an enhanced sensitivity (10-100 times greater than the wild type) to ethanol in growth medium, while it grows normally in the absence of ethanol, and responds normally to other alcohols and to environmental stresses such as heat shock and high salinity. The ethanol-hypersensitive phenotype of gek1 requires alcohol dehydrogenase activity, indicating that gek1 is sensitive not to ethanol itself but to the metabolites of ethanol. Consistent with this, gek1 shows enhanced sensitivity to acetaldehyde in the medium. The endogenous acetaldehyde levels were not different between gek1-2 and wild-type seedlings treated with ethanol. These results indicate that the ethanol hypersensitivity of gek1 is due to an enhanced sensitivity to acetaldehyde toxicity, instead of abnormally elevated accumulation of toxic acetaldehyde, which has been thought to be the major cause of ethanol toxicity in mammal cells.