Seattle Children's Research Institute, Seattle, WA 98101, USA.
Seattle Children's Research Institute, Seattle, WA 98101, USA; Department of Pediatrics, University of Washington, Seattle, WA 98195, USA; Brotman-Baty Institute for Precision Medicine, Seattle, WA 98195, USA.
Am J Hum Genet. 2020 Dec 3;107(6):1029-1043. doi: 10.1016/j.ajhg.2020.10.015. Epub 2020 Nov 16.
Genetic testing has increased the number of variants identified in disease genes, but the diagnostic utility is limited by lack of understanding variant function. CARD11 encodes an adaptor protein that expresses dominant-negative and gain-of-function variants associated with distinct immunodeficiencies. Here, we used a "cloning-free" saturation genome editing approach in a diploid cell line to simultaneously score 2,542 variants for decreased or increased function in the region of CARD11 associated with immunodeficiency. We also described an exon-skipping mechanism for CARD11 dominant-negative activity. The classification of reported clinical variants was sensitive (94.6%) and specific (88.9%), which rendered the data immediately useful for interpretation of seven coding and splicing variants implicated in immunodeficiency found in our clinic. This approach is generalizable for variant interpretation in many other clinically actionable genes, in any relevant cell type.
基因检测增加了疾病基因中变异的数量,但由于缺乏对变异功能的理解,其诊断效用有限。CARD11 编码一种衔接蛋白,表达与不同免疫缺陷相关的显性负性和功能获得性变异。在这里,我们在二倍体细胞系中使用了一种“无克隆”饱和基因组编辑方法,同时对与免疫缺陷相关的 CARD11 区域内的 2542 个变异进行了功能降低或增强的评分。我们还描述了 CARD11 显性负性活性的外显子跳跃机制。报告的临床变异的分类具有较高的敏感性(94.6%)和特异性(88.9%),这使得这些数据可立即用于解释我们临床发现的 7 个编码和剪接变异与免疫缺陷的相关性。这种方法可推广应用于许多其他具有临床可操作性的基因中的变异解释,以及任何相关的细胞类型。