Werner Ralf, Mönig Isabel, Lünstedt Ralf, Wünsch Lutz, Thorns Christoph, Reiz Benedikt, Krause Alexandra, Schwab Karl Otfried, Binder Gerhard, Holterhus Paul-Martin, Hiort Olaf
Department of Paediatrics and Adolescent Medicine, Division of Experimental Paediatric Endocrinology and Diabetes, University of Lübeck, Lübeck, Germany.
Department of Paediatric Surgery, University Hospital of Lübeck, Germany.
PLoS One. 2017 May 1;12(5):e0176720. doi: 10.1371/journal.pone.0176720. eCollection 2017.
Mutations in NR5A1 have been reported as a frequent cause of 46,XY disorders of sex development (DSD) associated to a broad phenotypic spectrum ranging from infertility, ambiguous genitalia, anorchia to gonadal dygenesis and female genitalia. Here we present the clinical follow up of four 46,XY DSD patients with three novel heterozygous mutations in the NR5A1 gene leading to a p.T40P missense mutation and a p.18DKVSG22del nonframeshift deletion in the DNA-binding domain and a familiar p.Y211Tfs*83 frameshift mutation. Functional analysis of the missense and nonframeshift mutation revealed a deleterious character with loss of DNA-binding and transactivation capacity. Both, the mutations in the DNA-binding domain, as well as the familiar frameshift mutation are associated with highly variable endocrine values and phenotypic appearance. Phenotypes vary from males with spontaneous puberty, substantial testosterone production and possible fertility to females with and without Müllerian structures and primary amenorrhea. Exome sequencing of the sibling's family revealed TBX2 as a possible modifier of gonadal development in patients with NR5A1 mutations.
据报道,NR5A1突变是46,XY性发育障碍(DSD)的常见病因,其相关表型谱广泛,包括不育、生殖器模糊、无睾症、性腺发育不全以及女性生殖器等。在此,我们报告了4例46,XY DSD患者的临床随访情况,这些患者在NR5A1基因中有3种新的杂合突变,导致p.T40P错义突变、DNA结合域中的p.18DKVSG22del非移码缺失以及家族性p.Y211Tfs*83移码突变。对该错义突变和非移码突变的功能分析显示其具有有害性,会导致DNA结合和反式激活能力丧失。DNA结合域中的突变以及家族性移码突变均与高度可变的内分泌值和表型外观相关。表型从具有自然青春期、大量睾酮分泌且可能具有生育能力的男性,到有或无苗勒管结构及原发性闭经的女性不等。对该患者兄弟姐妹家庭的外显子组测序显示,TBX2可能是NR5A1突变患者性腺发育的修饰基因。