Bashamboo Anu, Brauner Raja, Bignon-Topalovic Joelle, Lortat-Jacob Stephen, Karageorgou Vasiliki, Lourenco Diana, Guffanti Alessandro, McElreavey Ken
Human Developmental Genetics, Institut Pasteur, Paris, France
Université Paris Descartes and Pediatric Endocrinology Unit, Fondation Ophtalmologique Adolphe de Rothschild, Paris 75940, France.
Hum Mol Genet. 2014 Jul 15;23(14):3657-65. doi: 10.1093/hmg/ddu074. Epub 2014 Feb 18.
In recent years, considerable advances have been made in our understanding of genetics of mammalian gonad development; however, the underlying genetic aetiology in the majority of patients with 46,XY disorders of sex development (DSD) still remains unknown. Based on mouse models, it has been hypothesized that haploinsufficiency of the Friend of GATA 2 (FOG2) gene could lead to 46,XY gonadal dysgenesis on specific inbred genetic backgrounds. Using whole exome sequencing, we identified independent missense mutations in FOG2 in two patients with 46,XY gonadal dysgenesis. One patient carried a non-synonymous heterozygous mutation (p.S402R), while the other patient carried a heterozygous p.R260Q mutation and a homozygous p.M544I mutation. Functional studies indicated that the failure of testis development in these cases could be explained by the impaired ability of the mutant FOG2 proteins to interact with a known regulator of early testis development, GATA4. This is the first example of mutations in the coding sequence of FOG2 associated with 46,XY DSD in human and adds to the list of genes in the human known to be associated with DSD.
近年来,我们对哺乳动物性腺发育遗传学的理解取得了显著进展;然而,大多数46,XY性发育障碍(DSD)患者潜在的遗传病因仍然未知。基于小鼠模型,有人提出,在特定的近交遗传背景下,GATA 2之友(FOG2)基因的单倍剂量不足可能导致46,XY性腺发育不全。我们通过全外显子组测序,在两名46,XY性腺发育不全患者中鉴定出FOG2基因的独立错义突变。一名患者携带非同义杂合突变(p.S402R),而另一名患者携带杂合p.R260Q突变和纯合p.M544I突变。功能研究表明,这些病例中睾丸发育失败可以用突变的FOG2蛋白与已知的早期睾丸发育调节因子GATA4相互作用能力受损来解释。这是人类中与46,XY DSD相关的FOG2编码序列突变的首个例子,并增加了已知与DSD相关的人类基因列表。