Actl7a-KO Mouse

Actl7a, or Actin-like 7A, is essential for acrosome formation, fertilization and early embryo development [2]. It may be involved in pathways related to autophagy as indicated by proteomic analysis of testes from wild-type and Actl7a-KO mice, which showed differential gene expression enriched in the PI3K/AKT/mTOR signaling pathway [2]. Genetic models, such as the Actl7a knockout (KO) mouse model, are valuable for studying its functions.

In Actl7a-KO mice, deficiency leads to malformed sperm acrosomes, male infertility, reduced sperm-zona pellucida (ZP) binding ability, and abnormal localization of ZPBP in sperm, which may affect ZP binding [1]. The deletion of ACTL7A also damages the formation of the acrosome-acroplaxome-manchette complex, resulting in small-headed sperm [2]. Additionally, in misshapen sperm of Actl7a-KO mice, the localization and expression of the PLCZ1 protein are abnormal, leading to reduced calcium oscillations in oocytes [1].

In conclusion, Actl7a plays a crucial role in male fertility through its functions in acrosome formation and sperm-oocyte interaction. Studies using Actl7a-KO mouse models have revealed its significance in these processes, providing essential evidence for understanding male infertility and potential treatment strategies for patients suffering from infertility related to Actl7a mutations [1,2].

References:

1. Zhou, Xiaopei, Liu, Zhenxing, Jia, Weimin, Hou, Meiqi, Zhang, Xianqin. 2022. Actl7a deficiency in mice leads to male infertility and fertilization failure. In Biochemical and biophysical research communications, 623, 154-161. doi:10.1016/j.bbrc.2022.07.065. https://pubmed.ncbi.nlm.nih.gov/35921706/

2. Zhang, Yini, Tang, Jianan, Wang, Xuemei, Sun, Xiaoxi, Xin, Aijie. 2023. Loss of ACTL7A causes small head sperm by defective acrosome-acroplaxome-manchette complex. In Reproductive biology and endocrinology : RB&E, 21, 82. doi:10.1186/s12958-023-01130-5. https://pubmed.ncbi.nlm.nih.gov/37667331/