Singer-Berk Moriel, Gudmundsson Sanna, Baxter Samantha, Seaby Eleanor G, England Eleina, Wood Jordan C, Son Rachel G, Watts Nicholas A, Karczewski Konrad J, Harrison Steven M, MacArthur Daniel G, Rehm Heidi L, O'Donnell-Luria Anne
Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Center for Genomic Medicine & Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA.
medRxiv. 2023 Mar 9:2023.03.08.23286955. doi: 10.1101/2023.03.08.23286955.
Predicted loss of function (pLoF) variants are highly deleterious and play an important role in disease biology, but many of these variants may not actually result in loss-of-function. Here we present a framework that advances interpretation of pLoF variants in research and clinical settings by considering three categories of LoF evasion: (1) predicted rescue by secondary sequence properties, (2) uncertain biological relevance, and (3) potential technical artifacts. We also provide recommendations on adjustments to ACMG/AMP guidelines's PVS1 criterion. Applying this framework to all high-confidence pLoF variants in 22 autosomal recessive disease-genes from the Genome Aggregation Database (gnomAD, v2.1.1) revealed predicted LoF evasion or potential artifacts in 27.3% (304/1,113) of variants. The major reasons were location in the last exon, in a homopolymer repeat, in low per-base expression (pext) score regions, or the presence of cryptic splice rescues. Variants predicted to be potential artifacts or to evade LoF were enriched for ClinVar benign variants. PVS1 was downgraded in 99.4% (162/163) of LoF evading variants assessed, with 17.2% (28/163) downgraded as a result of our framework, adding to previous guidelines. Variant pathogenicity was affected (mostly from likely pathogenic to VUS) in 20 (71.4%) of these 28 variants. This framework guides assessment of pLoF variants beyond standard annotation pipelines, and substantially reduces false positive rates, which is key to ensure accurate LoF variant prediction in both a research and clinical setting.
预测功能丧失(pLoF)变异具有高度有害性,在疾病生物学中起着重要作用,但其中许多变异可能实际上并不会导致功能丧失。在此,我们提出了一个框架,通过考虑三类功能丧失规避情况,推进在研究和临床环境中对pLoF变异的解读:(1)由二级序列特性预测的挽救,(2)不确定的生物学相关性,以及(3)潜在的技术假象。我们还就调整美国医学遗传学与基因组学学会(ACMG)/美国分子病理学会(AMP)指南的PVS1标准提供了建议。将此框架应用于基因组聚合数据库(gnomAD,v2.1.1)中22个常染色体隐性疾病基因的所有高可信度pLoF变异,发现27.3%(304/1,113)的变异存在预测的功能丧失规避或潜在假象。主要原因是位于最后一个外显子、同聚物重复序列、低每碱基表达(pext)评分区域,或存在隐蔽性剪接挽救。预测为潜在假象或规避功能丧失的变异在ClinVar良性变异中富集。在评估的163个规避功能丧失的变异中,99.4%(162/163)的PVS1被降级,其中17.2%(28/163)因我们的框架而降级,这是对先前指南的补充。在这28个变异中,20个(71.4%)的变异致病性受到影响(大多从可能致病变为意义未明的变异)。该框架指导了超出标准注释流程的pLoF变异评估,并大幅降低了假阳性率,这对于在研究和临床环境中确保准确的功能丧失变异预测至关重要。