Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06520, USA.
Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06520, USA.
Science. 2013 Oct 4;342(6154):1235587. doi: 10.1126/science.1235587.
Interpreting variants, especially noncoding ones, in the increasing number of personal genomes is challenging. We used patterns of polymorphisms in functionally annotated regions in 1092 humans to identify deleterious variants; then we experimentally validated candidates. We analyzed both coding and noncoding regions, with the former corroborating the latter. We found regions particularly sensitive to mutations ("ultrasensitive") and variants that are disruptive because of mechanistic effects on transcription-factor binding (that is, "motif-breakers"). We also found variants in regions with higher network centrality tend to be deleterious. Insertions and deletions followed a similar pattern to single-nucleotide variants, with some notable exceptions (e.g., certain deletions and enhancers). On the basis of these patterns, we developed a computational tool (FunSeq), whose application to ~90 cancer genomes reveals nearly a hundred candidate noncoding drivers.
解析越来越多的个人基因组中的变异,尤其是非编码变异,极具挑战性。我们利用 1092 个人类个体中功能注释区域的多态性模式,来识别有害变异;然后通过实验验证候选变异。我们分析了编码和非编码区域,前者为后者提供了佐证。我们发现了一些特别容易发生突变的区域(“超敏区”),以及由于对转录因子结合的机制性影响而导致破坏的变异(即“基序破坏者”)。我们还发现,网络中心性较高的区域中的变异往往是有害的。插入和缺失遵循与单核苷酸变异相似的模式,但也有一些显著的例外(例如,某些缺失和增强子)。基于这些模式,我们开发了一种计算工具(FunSeq),该工具应用于大约 90 个癌症基因组,揭示了近 100 个候选非编码驱动因子。