Yang Shulin, Li Zongzhe, Ren Xinling, Yue Jing
Reproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Division of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Reprod Sci. 2025 May;32(5):1557-1565. doi: 10.1007/s43032-024-01729-y. Epub 2024 Oct 23.
The oocyte maturation defect 6 is an autosomal recessive hereditary disease caused by a homozygous variant in ZP2 gene. It is characterized by female primary infertility due to an abnormally thin zona pellucida (ZP) and defective sperm binding. Here we identified a compound heterozygous variant (c.1924C > T and c.1695-2A > G) in ZP2 gene in a Chinese Han family. Quantitative real-time PCR showed that the variant c.1924C > T significantly decreased the expression of truncated ZP2 message RNA by the nonsense-mediated decay pathway. Minigene assays showed the c.1695-2A > G variant led to an extra-61-nt preservation of intron 15 at the junction between exons 15 and 16 during transcription. Both variants (c.1924C > T and c.1695-2A > G) resulted in truncated ZP2 proteins (p.R642X and p.C566Hfs*2) that lost the transmembrane domain, which prevented the secretion of the mutant ZP2 proteins and produced a structurally abnormal ZP, thus resulting in female infertility. This study further elucidated the pathogenic mechanism of these two variants and provided new support for the genetic diagnosis of female infertility.
卵母细胞成熟缺陷6是一种常染色体隐性遗传病,由ZP2基因的纯合变异引起。其特征是由于透明带(ZP)异常变薄和精子结合缺陷导致女性原发性不孕。在此,我们在中国汉族一个家系中鉴定出ZP2基因的一个复合杂合变异(c.1924C>T和c.1695-2A>G)。定量实时PCR显示,c.1924C>T变异通过无义介导的衰变途径显著降低了截短的ZP2信使RNA的表达。小基因检测显示,c.1695-2A>G变异导致转录过程中外显子15和16交界处内含子15额外保留61个核苷酸。这两个变异(c.1924C>T和c.1695-2A>G)均导致截短的ZP2蛋白(p.R642X和p.C566Hfs*2)丢失跨膜结构域,这阻止了突变ZP2蛋白的分泌并产生结构异常的ZP,从而导致女性不孕。本研究进一步阐明了这两个变异的致病机制,为女性不孕的基因诊断提供了新的支持。