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Azacytidine-induced reactivation of a DNA repair gene in Chinese hamster ovary cells.

机译:氮杂胞苷诱导的中国仓鼠卵巢细胞中DNA修复基因的激活。

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Six X-ray-sensitive (xrs) strains of the CHO-K1 cell line were shown to revert at a very high frequency after treatment with 5-azacytidine. This suggested that there was a methylated xrs+ gene in these strains which was structurally intact, but not expressed. The xrs strains did not complement one another, and the locus was autosomally located. In view of the frequency of their isolation and their somewhat different phenotypes, we propose that the xrs strains are mutants derived from an active wild-type gene. However, there is in addition a methylated silent gene present in the genome. Azacytidine treatment reactivated this gene. We present a model for the functional hemizygosity of mammalian cell lines, which is based on the inactivation of genes by de novo hypermethylation. In contrast to results with xrs strains, other repair-defective lines were found not to be reverted by azacytidine.
机译:在使用5-氮杂胞苷处理后,CHO-K1细胞系的六种X射线敏感(xrs)菌株显示出很高的回复频率。这表明在这些菌株中存在甲基化的xrs +基因,该基因在结构上是完整的,但是没有表达。 xrs菌株彼此不互补,并且基因座是自体定位的。考虑到它们的分离频率和它们有些不同的表型,我们建议xrs菌株是衍生自活性野生型基因的突变体。但是,基因组中还存在一个甲基化的沉默基因。氮杂胞苷处理使该基因重新激活。我们提出了哺乳动物细胞系功能性半合子性的模型,该模型基于通过从头甲基化使基因失活。与xrs菌株的结果相反,发现氮杂胞苷不能还原其他修复缺陷品系。

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