Cappato Serena, Divizia Maria Teresa, Menta Ludovica, Rosti Giulia, Puliti Aldamaria, Martinheira Da Silva Joana Soraia, Santamaria Giuseppe, Di Duca Marco, Ronchetto Patrizia, Faravelli Francesca, Zara Federico, Bocciardi Renata
Medical Genetics Unit, IRCCS Istituto Giannina Gaslini, Genoa, Italy.
Genomics and Clinical Genetics Unit, IRCCS Istituto Giannina Gaslini, Genoa, Italy.
NPJ Genom Med. 2025 Feb 12;10(1):10. doi: 10.1038/s41525-024-00460-6.
Nail-Patella syndrome (NPS) is a rare autosomal dominant condition due to haploinsufficiency of LMX1B, caused by loss-of-function variants affecting the coding sequence, or partial/whole deletions of the gene. In here, we describe two familial cases of NPS, carrying novel variants of the LMX1B 5'UTR region (-174C>T and -226G>A). To verify their pathogenic role, we carried out a functional characterization, both by reporter gene assays in heterologous systems and in patient's derived cells. We demonstrated that both variants impair LMX1B expression at post-transcriptional level. They introduce two upstream open reading frames (uORFs), out-of-frame with the main LMX1B coding sequence, generating transcripts detected by the non-sense mediated decay (NMD). We also demonstrated that the escape of the altered mRNA from NMD, if any, may lead to the synthesis of an aberrant LMX1B protein.
指甲-髌骨综合征(NPS)是一种罕见的常染色体显性疾病,由影响编码序列的功能丧失变异或该基因的部分/全部缺失导致LMX1B单倍剂量不足引起。在此,我们描述了两例携带LMX1B 5'UTR区域新变异(-174C>T和-226G>A)的NPS家族病例。为了验证它们的致病作用,我们通过异源系统中的报告基因分析以及患者来源的细胞进行了功能表征。我们证明这两种变异均在转录后水平损害LMX1B的表达。它们引入了两个上游开放阅读框(uORF),与主要的LMX1B编码序列框外,产生了由无义介导的衰变(NMD)检测到的转录本。我们还证明,改变后的mRNA从NMD逃逸(如果有的话)可能导致异常LMX1B蛋白的合成。