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首页> 外文期刊>Molecular and Cellular Biology >Incubation at the nonpermissive temperature induces deficiencies in UV resistance and mutagenesis in mouse mutant cells expressing a temperature-sensitive ubiquitin-activating enzyme (E1).
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Incubation at the nonpermissive temperature induces deficiencies in UV resistance and mutagenesis in mouse mutant cells expressing a temperature-sensitive ubiquitin-activating enzyme (E1).

机译：在不允许的温度下温育会诱导表达温度敏感性泛素激活酶（E1）的小鼠突变细胞的抗紫外线性和诱变能力不足。

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In temperature-sensitive (ts) mutants of mouse FM3A cells, the levels of mutagenesis and survival of cells treated with DNA-damaging agents have been difficult to assess because they are killed after their mutant phenotypes are expressed at the nonpermissive temperature. To avoid this difficulty, we incubated the ts mutant cells at the restrictive temperature, 39 degrees C, for only a limited period after inducing DNA damage. We used ts mutants defective in genes for ubiquitin-activating enzyme (E1), DNA polymerase alpha, and p34(cdc2) kinase. Whereas the latter two showed no effect, E1 mutants were sensitized remarkably to UV light if incubated at 39 degrees C for limited periods after UV exposure. Eighty-five percent of the sensitization occurred within the first 12 h of incubation at 39 degrees C, and more than 36 h at 39 degrees C did not produce any further sensitization. Moreover, while the 39 degrees C incubation gave E1 mutants a moderate spontaneous mutator phenotype, the same treatment significantly diminished the level of UV-induced 6-thioguanine resistance mutagenesis and extended the time necessary for expression of the mutation phenotype. These characteristics of E1 mutants are reminiscent of the defective DNA repair phenotypes of Saccharomyces cerevisiae rad6 mutants, which have defects in a ubiquitin-conjugating enzyme (E2), to which E1 is known to transfer ubiquitin. These results demonstrate the involvement of E1 in eukaryotic DNA repair and mutagenesis and provide the first direct evidence that the ubiquitin-conjugation system contributes to DNA repair in mammalian cells.
机译：在小鼠FM3A细胞的温度敏感型（ts）突变体中，用DNA损伤剂处理过的细胞的诱变水平和存活率难以评估，因为它们的突变型在非容许温度下表达后被杀死。为避免这种困难，我们在诱导DNA损伤后仅在有限的时间内将ts突变型细胞在39摄氏度的限制温度下孵育。我们使用了在遍在蛋白激活酶（E1），DNA聚合酶α和p34（cdc2）激酶基因缺陷的ts突变体。尽管后两个没有作用，但是如果在紫外线照射后在39摄氏度下孵育E1突变体，E1突变体将对紫外线显着敏感。百分之八十五的致敏发生在39摄氏度的孵育的前12小时内，在39摄氏度下超过36个小时没有产生任何进一步的敏化作用。此外，尽管在39摄氏度的温育下，E1突变体具有中等程度的自发突变体表型，但相同的处理方法显着降低了UV诱导的6-硫鸟嘌呤抗性诱变的水平，并延长了表达突变表型所需的时间。 E1突变体的这些特征使人联想到酿酒酵母rad6突变体的缺陷DNA修复表型，后者在泛素结合酶（E2）中存在缺陷，已知E1会向该酶转移泛素。这些结果表明E1参与真核DNA修复和诱变，并提供了第一个直接证据，表明泛素结合系统有助于哺乳动物细胞中的DNA修复。

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