Ghoshal K, Li Z, Jacob S T
Department of Medical Biochemistry, The Ohio State University, College of Medicine, 333 Hamilton Hall, 1645 Neil Avenue, Columbus, OH 43210, USA.
Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10390-5. doi: 10.1073/pnas.95.18.10390.
Metallothioneins (MT) are involved in the scavenging of the toxic heavy metals and protection of cells from reactive oxygen intermediates. To investigate the potential role of the protein Ku in the expression of MT, we measured the level of MT-I mRNA in the parental rat fibroblast cell line (Rat 1) and the cell lines that stably and constitutively overexpress the small subunit, the large subunit, and the heterodimer of Ku. Treatment with CdS04 or ZnS04 elevated the MT-I mRNA level 20- to 30-fold in the parental cells and the cells (Ku-70) that overproduce the small subunit or those (Ku-7080) overexpressing the heterodimer. By contrast, the cells (Ku-80) overexpressing the large subunit of Ku failed to induce MT-I. In vitro transcription assay showed that the MT-I promoter activity was suppressed selectively in the nuclear extracts from Ku-80 cells. The specificity of the repressor function was shown by the induction of hsp 70, another Cd-inducible gene, in Ku-80 cells. Addition of the nuclear extract from Ku-80 cells at the start of the transcription reaction abolished the MT-l promoter activity in the Rat 1 cell extract. The transcript once formed in Rat 1 nuclear extract was not degraded by further incubation with the extract from Ku-80 cells. The repressor was sensitive to heat. The DNA-binding activities of at least four transcription factors that control the MT-I promoter activity were not affected in Ku-80 cells. These observations have set the stage for further exploration of the mechanisms by which the Ku subunit mediates suppression of MT induction.
金属硫蛋白(MT)参与清除有毒重金属并保护细胞免受活性氧中间体的损伤。为了研究蛋白质Ku在MT表达中的潜在作用,我们测量了亲代大鼠成纤维细胞系(Rat 1)以及稳定且组成性过表达Ku小亚基、大亚基和异二聚体的细胞系中MT-I mRNA的水平。用CdS04或ZnS04处理后,亲代细胞以及过量产生小亚基的细胞(Ku-70)或过量表达异二聚体的细胞(Ku-7080)中MT-I mRNA水平升高了20至30倍。相比之下,过量表达Ku大亚基的细胞(Ku-80)未能诱导MT-I。体外转录分析表明,MT-I启动子活性在Ku-80细胞的核提取物中被选择性抑制。另一个镉诱导基因hsp 70在Ku-80细胞中的诱导显示了阻遏物功能的特异性。在转录反应开始时添加Ku-80细胞的核提取物消除了Rat 1细胞提取物中MT-1启动子的活性。在Rat 1核提取物中一旦形成的转录本不会因与Ku-80细胞提取物进一步孵育而降解。该阻遏物对热敏感。在Ku-80细胞中,至少四种控制MT-I启动子活性的转录因子的DNA结合活性未受影响。这些观察结果为进一步探索Ku亚基介导MT诱导抑制的机制奠定了基础。