Department of Neuroscience, Department of Developmental and Regenerative Biology, Department of Neurosurgery, Icahn School of Medicine at Mount, Sinai, New York, New York, United States of America.
PLoS One. 2013 Aug 5;8(8):e72338. doi: 10.1371/journal.pone.0072338. Print 2013.
Somatic transposon mutagenesis in mice is an efficient strategy to investigate the genetic mechanisms of tumorigenesis. The identification of tumor driving transposon insertions traditionally requires the generation of large tumor cohorts to obtain information about common insertion sites. Tumor driving insertions are also characterized by their clonal expansion in tumor tissue, a phenomenon that is facilitated by the slow and evolving transformation process of transposon mutagenesis. We describe here an improved approach for the detection of tumor driving insertions that assesses the clonal expansion of insertions by quantifying the relative proportion of sequence reads obtained in individual tumors. To this end, we have developed a protocol for insertion site sequencing that utilizes acoustic shearing of tumor DNA and Illumina sequencing. We analyzed various solid tumors generated by PiggyBac mutagenesis and for each tumor >10⁶ reads corresponding to >10⁴ insertion sites were obtained. In each tumor, 9 to 25 insertions stood out by their enriched sequence read frequencies when compared to frequencies obtained from tail DNA controls. These enriched insertions are potential clonally expanded tumor driving insertions, and thus identify candidate cancer genes. The candidate cancer genes of our study comprised many established cancer genes, but also novel candidate genes such as Mastermind-like1 (Mamld1) and Diacylglycerolkinase delta (Dgkd). We show that clonal expansion analysis by high-throughput sequencing is a robust approach for the identification of candidate cancer genes in insertional mutagenesis screens on the level of individual tumors.
体细胞转座子诱变在小鼠中是一种研究肿瘤发生遗传机制的有效策略。传统上,鉴定肿瘤驱动转座子插入需要生成大量肿瘤队列,以获得有关常见插入位点的信息。肿瘤驱动插入还以其在肿瘤组织中的克隆扩增为特征,这种现象是由转座子诱变的缓慢和进化的转化过程促进的。我们在这里描述了一种改进的检测肿瘤驱动插入的方法,该方法通过定量个体肿瘤中获得的序列读取的相对比例来评估插入的克隆扩增。为此,我们开发了一种插入位点测序方案,该方案利用肿瘤 DNA 的声学剪切和 Illumina 测序。我们分析了由 PiggyBac 诱变产生的各种实体瘤,对于每个肿瘤,获得了超过 10⁶个对应于超过 10⁴个插入位点的读取。在每个肿瘤中,与来自尾巴 DNA 对照的频率相比,有 9 到 25 个插入的序列读取频率富集。这些富集的插入是潜在的克隆扩增的肿瘤驱动插入,因此鉴定候选癌症基因。我们研究的候选癌症基因包括许多已确立的癌症基因,但也包括新的候选基因,如 Mastermind-like1 (Mamld1)和二酰基甘油激酶 delta (Dgkd)。我们表明,通过高通量测序进行的克隆扩增分析是在个体肿瘤水平上进行插入诱变筛选中鉴定候选癌症基因的一种稳健方法。