Zhou Xiaopei, Xi Qingsong, Jia Weimin, Li Zhou, Liu Zhenxing, Luo Geng, Xing Chenxi, Zhang Dazhi, Hou Meiqi, Liu Huihui, Yang Xue, Luo Yalin, Peng Xuejie, Wang Guihua, Zou Tingting, Zhu Lixia, Jin Lei, Zhang Xianqin
Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, 430074, Hubei, China.
Reproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Mol Genet Genomics. 2023 Mar;298(2):353-360. doi: 10.1007/s00438-022-01985-0. Epub 2022 Dec 27.
Male infertility, a global public health problem, exhibits complex pathogenic causes and genetic factors deserve further discovery and study. We identified a novel homozygous missense mutation c.224A > C (p.D75A) in ACTL7A gene in two infertile brothers with teratozoospermia by whole-exome sequencing (WES). In vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI) showed fertilization failure of the two affected couples. The three-dimensional (3D) models showed that a small section of α-helix transformed into random coil in the mutant ACTL7A protein and mutant amino acid lacked a hydrogen bond with Ser170 amino acid. Immunofluorescence revealed that ACTL7A protein was degraded in sperms of patients. Transmission electron microscopy (TEM) analysis of sperms from the infertile patients showed that the irregular perinuclear theca (PT) and acrosomal ultrastructural defects. Furthermore, ACTL7A mutation caused abnormal localization and reduced the expression of PLCZ1 in sperms of the patients, which may be the key reasons for the fertilization failure after ICSI. Our findings expand the spectrum of ACTL7A mutations and provide novel theoretical basis for genetic counseling.
男性不育是一个全球性的公共卫生问题,其致病原因复杂,遗传因素值得进一步探索和研究。我们通过全外显子组测序(WES)在两名患有畸形精子症的不育兄弟中,于ACTL7A基因中鉴定出一种新的纯合错义突变c.224A>C(p.D75A)。体外受精(IVF)和卵胞浆内单精子注射(ICSI)显示,这两对受影响夫妇均受精失败。三维(3D)模型显示,突变型ACTL7A蛋白中有一小段α-螺旋转变为无规卷曲,且突变氨基酸与Ser170氨基酸之间缺乏氢键。免疫荧光显示,患者精子中的ACTL7A蛋白发生降解。对不育患者精子进行透射电子显微镜(TEM)分析显示,核周致密纤维层(PT)不规则,顶体超微结构存在缺陷。此外,ACTL7A突变导致患者精子中PLCZ1定位异常并使其表达降低,这可能是ICSI后受精失败的关键原因。我们的研究结果拓宽了ACTL7A突变谱,为遗传咨询提供了新的理论依据。