Kobayashi T, Urakami S, Hirayama Y, Yamamoto T, Nishizawa M, Takahara T, Kubo Y, Hino O
Department of Experimental Pathology, Cancer Institute, Tokyo.
Jpn J Cancer Res. 1997 Mar;88(3):254-61. doi: 10.1111/j.1349-7006.1997.tb00375.x.
We searched for the rat homologue of the human tuberous sclerosis (TSC2) gene mutations in loss of heterozygosity (LOH)-negative Eker rat renal carcinomas (RCs) by polymerase chain reaction-single-strand conformational polymorphism (PCR-SSCP) analysis using 45 primer sets covering all 41 coding exons and one leader exon including splicing donor/acceptor sites. We have identified intragenic somatic mutations in 7 of 21 spontaneous RCs, including one cell line (33%), and in 3 of 9 (33%) N-ethyl-N-nitrosourea (ENU)-induced LOH-negative RCs. Interestingly, five mutations in the spontaneous RCs were either deletion or duplication (5/7 = 71%). In contrast, all three in ENU-induced RCs were base substitutions (3/3 = 100%), as expected. Thus, a qualitative difference in the second hit might exist between spontaneous and ENU-induced mutations (e.g., deletion or duplication versus point mutation). By a direct cloning approach utilizing the restriction length difference caused by germline insertional mutation or reverse transcriptase-PCR analysis in two applicable cases, we could clearly show the presence of intragenic somatic mutations in the second copy (wild-type) of the Tsc2 gene. This is the first demonstration at the DNA sequence level of the validity of Knudson's two-hits hypothesis in the Tsc2 gene.
我们使用覆盖所有41个编码外显子和一个包含剪接供体/受体位点的前导外显子的45对引物,通过聚合酶链反应-单链构象多态性(PCR-SSCP)分析,在杂合性缺失(LOH)阴性的Eker大鼠肾癌(RC)中寻找人类结节性硬化症(TSC2)基因突变的大鼠同源物。我们在21个自发RC中的7个(包括一个细胞系,占33%)以及9个N-乙基-N-亚硝基脲(ENU)诱导的LOH阴性RC中的3个(占33%)中鉴定出基因内体细胞突变。有趣的是,自发RC中的5个突变是缺失或重复(5/7 = 71%)。相比之下,正如预期的那样,ENU诱导的RC中的所有3个突变都是碱基替换(3/3 = 100%)。因此,自发突变和ENU诱导的突变在第二次打击中可能存在质的差异(例如,缺失或重复与点突变)。在两个适用的案例中,通过利用种系插入突变引起的限制性长度差异的直接克隆方法或逆转录酶-PCR分析,我们能够清楚地显示Tsc2基因第二个拷贝(野生型)中存在基因内体细胞突变。这是在DNA序列水平上首次证明Knudson的两次打击假说在Tsc2基因中的有效性。