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P53基因缺陷不会增强正常组织体细胞中小鼠微卫星的不稳定性。

P53 gene deficiency does not enhance instability of mouse minisatellites in somatic cells of normal tissues.

作者信息

Ohashi M, Hatakeyama K, Aizawa S, Kominami R

机构信息

First Department of Biochemistry, Niigata University School of Medicine.

出版信息

Jpn J Cancer Res. 1996 Jul;87(7):696-701. doi: 10.1111/j.1349-7006.1996.tb00280.x.

Abstract

The effect of p53-deficiency on somatic mutation of minisatellites in normal tissues was examined using p53-deficient (-/-) mice. In total, 248 mice consisting of three different genotypes, +/+, +/ -and -/-, were obtained and DNA from their embryos was probed with two minisatellites, Pc-1 and Pc-2. The somatic mutation was detected by Southern blot hybridization as the presence of a third nonparental band reflecting mosaicism in tissues. Mutation frequency of Pc-1 for (+/+) and (+/-) was 1.3% and 1.4%, respectively, which is consistent with previous studies. On the other hand, none of the mice lacking the p53 gene (-/-) exhibited mutation. The Pc-2 probe did not show any somatic mutation in the three groups. These results suggest that the p53 deficiency does not enhance the genomic instability of the minisatellite loci in normal somatic cells.

摘要

利用p53基因缺陷型(-/-)小鼠,研究了p53基因缺陷对正常组织中微卫星体细胞突变的影响。总共获得了248只具有三种不同基因型(+/+、+/-和-/-)的小鼠,并用两种微卫星Pc-1和Pc-2对其胚胎DNA进行检测。通过Southern印迹杂交检测体细胞突变,以反映组织中嵌合体的第三条非亲本条带的存在。(+/+)和(+/-)小鼠中Pc-1的突变频率分别为1.3%和1.4%,这与先前的研究结果一致。另一方面,缺乏p53基因的小鼠(-/-)均未表现出突变。Pc-2探针在三组中均未显示任何体细胞突变。这些结果表明,p53基因缺陷不会增强正常体细胞中微卫星位点的基因组不稳定性。

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