Department of Pediatrics, Inselspital, Pediatric Endocrinology, Diabetology and Metabolism, Bern University Hospital, University of Bern, Bern, Switzerland.
Department for BioMedical Research, University of Bern, Bern, Switzerland.
PLoS One. 2023 Jul 11;18(7):e0287515. doi: 10.1371/journal.pone.0287515. eCollection 2023.
NR5A1/SF-1 (Steroidogenic factor-1) variants may cause mild to severe differences of sex development (DSD) or may be found in healthy carriers. The NR5A1/SF-1 c.437G>C/p.Gly146Ala variant is common in individuals with a DSD and has been suggested to act as a susceptibility factor for adrenal disease or cryptorchidism. Since the allele frequency is high in the general population, and the functional testing of the p.Gly146Ala variant revealed inconclusive results, the disease-causing effect of this variant has been questioned. However, a role as a disease modifier is still possible given that oligogenic inheritance has been described in patients with NR5A1/SF-1 variants. Therefore, we performed next generation sequencing (NGS) in 13 DSD individuals harboring the NR5A1/SF-1 p.Gly146Ala variant to search for other DSD-causing variants and clarify the function of this variant for the phenotype of the carriers. Panel and whole-exome sequencing was performed, and data were analyzed with a filtering algorithm for detecting variants in NR5A1- and DSD-related genes. The phenotype of the studied individuals ranged from scrotal hypospadias and ambiguous genitalia in 46,XY DSD to opposite sex in both 46,XY and 46,XX. In nine subjects we identified either a clearly pathogenic DSD gene variant (e.g. in AR) or one to four potentially deleterious variants that likely explain the observed phenotype alone (e.g. in FGFR3, CHD7). Our study shows that most individuals carrying the NR5A1/SF-1 p.Gly146Ala variant, harbor at least one other deleterious gene variant which can explain the DSD phenotype. This finding confirms that the NR5A1/SF-1 p.Gly146Ala variant may not contribute to the pathogenesis of DSD and qualifies as a benign polymorphism. Thus, individuals, in whom the NR5A1/SF-1 p.Gly146Ala gene variant has been identified as the underlying genetic cause for their DSD in the past, should be re-evaluated with a NGS method to reveal the real genetic diagnosis.
NR5A1/SF-1(类固醇生成因子-1)变体可能导致轻度至重度性别发育障碍(DSD),也可能存在于健康携带者中。NR5A1/SF-1 c.437G>C/p.Gly146Ala 变体在 DSD 患者中很常见,并且被认为是肾上腺疾病或隐睾的易感因素。由于该等位基因频率在普通人群中较高,且对 p.Gly146Ala 变体的功能测试结果不确定,因此该变体的致病作用受到质疑。然而,鉴于已在 NR5A1/SF-1 变体患者中描述了寡基因遗传,该变体仍可能作为疾病修饰因子发挥作用。因此,我们对 13 名携带 NR5A1/SF-1 p.Gly146Ala 变体的 DSD 个体进行了下一代测序(NGS),以寻找其他导致 DSD 的变体,并阐明该变体对携带者表型的功能。进行了面板和全外显子组测序,并使用一种用于检测 NR5A1-和 DSD 相关基因中的变体的过滤算法来分析数据。研究个体的表型范围从 46,XY DSD 的阴囊型尿道下裂和生殖器模糊到 46,XY 和 46,XX 的两性畸形。在 9 名受试者中,我们要么确定了明显的致病性 DSD 基因变体(例如 AR 中的变体),要么确定了一个至四个可能单独解释观察到的表型的有害变体(例如 FGFR3、CHD7 中的变体)。我们的研究表明,携带 NR5A1/SF-1 p.Gly146Ala 变体的大多数个体至少携带另一个可能导致 DSD 表型的有害基因变体。这一发现证实 NR5A1/SF-1 p.Gly146Ala 变体可能不会导致 DSD 的发病机制,并且符合良性多态性的标准。因此,过去曾将 NR5A1/SF-1 p.Gly146Ala 基因变体确定为其 DSD 遗传原因的个体,应使用 NGS 方法重新评估,以揭示真正的遗传诊断。