Overexpression of KAT8 induces a failure in early embryonic development in mice

胚胎干细胞 标记法 细胞生物学 胚泡 末端脱氧核苷酸转移酶 胚胎发生 生物 免疫染色 细胞凋亡 分子生物学 遗传学 胚胎 基因 免疫学 免疫组织化学
作者
Xuan Wu,Shiwei Wang,Yajun Guo,Shenming Zeng
出处
期刊:Theriogenology [Elsevier]
卷期号:221: 31-37
标识
DOI:10.1016/j.theriogenology.2024.03.014
摘要

Embryo quality is strongly associated with subsequent embryonic developmental efficiency. However, the detailed function of lysine acetyltransferase 8 (KAT8) during early embryonic development in mice remains elusive. In this study, we reported that KAT8 played a pivotal role in the first cleavage of mouse embryos. Immunostaining results revealed that KAT8 predominantly accumulated in the nucleus throughout the entire embryonic developmental process. Kat8 overexpression (Kat8-OE) was correlated with early developmental potential of embryos to the blastocyst stage. We also found that Kat8-OE embryos showed spindle-assembly defects and chromosomal misalignment, and that Kat8-OE in embryos led to increased levels of reactive oxygen species (ROS), accumulation of phosphorylated γH2AX by affecting the expression of critical genes related to mitochondrial respiratory chain and antioxidation pathways. Subsequently, cellular apoptosis was activated as confirmed by TUNEL (Terminal Deoxynucleotidyl Transferase mediated dUTP Nick-End Labeling) assay. Furthermore, we revealed that KAT8 was related to regulating the acetylation status of H4K16 in mouse embryos, and Kat8-OE induced the hyperacetylation of H4K16, which might be a key factor for the defective spindle/chromosome apparatus. Collectively, our data suggest that KAT8 constitutes an important regulator of spindle assembly and redox homeostasis during early embryonic development in mice.
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