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Increase in UV mutagenesis by heat stress on UV-irradiated E. coli cells.

机译:通过紫外线辐照大肠杆菌细胞的热应激增加UV诱变。

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摘要

When leu- auxotrophs of Escherichia coli, after UV irradiation, were grown at temperatures between 30 and 47°C, the frequency of UV-induced mutation from leu- to leu+ revertant increased as the UV dose and the temperature increased. For cells exposed to a UV dose of 45 J/m2, the mutation frequency at 47°C was 1.9 times that at 30°C; for a dose of 90 J/m2, it was 3.25 times; and for 135 J/m2, it was 4.8 times. Similar enhancement of reversion frequency was observed when the irradiated cells were grown at 30°C in the presence of a heat shock inducer, ethanol (8% v/v). Heat shock-mediated enhancement of UV mutagenesis did not occur in an E. coli mutant sigma 32 (heat shock regulator protein), but sigma 32 overexpression in the mutant strain (transformed with a sigma 32-bearing plasmid) increased the UV-induced mutation frequency. These results suggest that heat stress alone has no mutagenic property, but when applied to UV-damaged cells, it enhances the UV-induced frequency of cell mutation.
机译:当紫外线照射后的大肠杆菌的Leu-助剂在30至47℃之间的温度下生长,随着UV剂量和温度增加,Leu-in Leu + Reur + Revertant的UV诱导突变的频率增加。对于暴露于UV剂量为45J / m 2的细胞,47℃的突变频率在30℃下为1.9倍;对于90 J / M2的剂量,它为3.25倍;并且对于135 J / M2,它是4.8倍。当在热休克诱导剂的存在下在30℃下在乙醇(8%v / v)存在时,观察到辐照细胞在30℃下培养时,观察到类似的增强。在大肠杆菌突变体Sigma 32(热休克调节剂蛋白)中没有发生紫外线诱变的热冲击介导的增强,但突变菌株中的Sigma 32过表达(用Sigma 32-轴承质粒转化)增加了UV诱导的突变频率。这些结果表明,单独的热应力没有诱变性质,而是当施加到紫外线损伤的细胞时,它增强了紫外线诱导的细胞突变频率。

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