Key Laboratory of Zoonosis Research, Ministry of Education, College of Animal Sciences, Jilin University, Changchun 130062, China.
Key Laboratory of Zoonosis Research, Ministry of Education, College of Animal Sciences, Jilin University, Changchun 130062, China; Chongqing Research Institute, Jilin University, Chongqing 401120, China; Chongqing Jitang Biotechnology Research Institute Co., Ltd., Chongqing 401120, China.
Gene. 2023 Oct 20;883:147684. doi: 10.1016/j.gene.2023.147684. Epub 2023 Aug 1.
Dominant genetic variants in the mitofusin 2 (MFN2) gene lead to Charcot-Marie-Tooth type 2A (CMT2A), a neurodegenerative disease caused by genetic defects that directly damage axons. In this study, we reported a proband with a pathogenic variant in the GTPase domain of MFN2, c.494A > G (p.His165Arg). To date, at least 184 distinct MFN2 variants identified in 944 independent probands have been reported in 131 references. However, the field of medical genetics has long been challenged by how genetic variation in the MFN2 gene is associated with disease phenotypes. Here, by collating the MFN2 variant data and patient clinical information from Leiden Open Variant Database 3.0, NCBI clinvar database, and available related references in PubMed, we determined the mutation frequency, age of onset, sex ratio, and geographical distribution. Furthermore, the results of an analysis examining the relationship between variants and phenotypes from multiple genetic perspectives indicated that insertion and deletions (indels), copy number variants (CNVs), duplication variants, and nonsense mutations in single nucleotide variants (SNVs) tend to be pathogenic, and the results emphasized the importance of the GTPase domain to the structure and function of MFN2. Overall, three reliable classification methods of MFN2 genotype-phenotype associations provide insights into the prediction of CMT2A disease severity. Of course, there are still many MFN2 variants that have not been given clear clinical significance, which requires clinicians to make more accurate clinical diagnoses.
导致遗传性运动感觉神经病 2A 型(CMT2A)的主要遗传变异位于线粒体融合蛋白 2(MFN2)基因中,这是一种由直接损伤轴突的遗传缺陷引起的神经退行性疾病。在这项研究中,我们报告了一例 MFN2 基因 GTP 酶结构域致病性变异的先证者,c.494A>G(p.His165Arg)。迄今为止,在 131 篇参考文献中,已经在 944 例独立先证者中报道了至少 184 种不同的 MFN2 变异。然而,医学遗传学领域长期以来一直受到挑战,即 MFN2 基因的遗传变异如何与疾病表型相关。在这里,通过整理 Leiden Open Variant Database 3.0、NCBI clinvar 数据库和 PubMed 中可用的相关参考文献中的 MFN2 变异数据和患者临床信息,我们确定了突变频率、发病年龄、性别比和地理分布。此外,从多个遗传角度分析变异与表型之间关系的结果表明,插入和缺失(indels)、拷贝数变异(CNVs)、重复变异和单核苷酸变异(SNVs)中的无义突变倾向于具有致病性,结果强调了 GTP 酶结构域对 MFN2 结构和功能的重要性。总体而言,三种可靠的 MFN2 基因型-表型关联分类方法为预测 CMT2A 疾病严重程度提供了思路。当然,仍然有许多 MFN2 变异尚未给出明确的临床意义,这需要临床医生做出更准确的临床诊断。