Involvement of LIMK1/2 in actin assembly during mouse embryo development

被引:9
|
作者
Duan, Xing [1 ]
Zhang, Hao-Lin [1 ]
Wu, Lan-Lan [1 ]
Liu, Meng-Yao [1 ]
Pan, Meng-Hao [1 ]
Ou, Xiang-Hong [2 ]
Sun, Shao-Chen [1 ]
机构
[1] Nanjing Agr Univ, Coll Anim Sci & Technol, Nanjing, Jiangsu, Peoples R China
[2] Guangdong Second Prov Gen Hosp, Reprod Med Ctr, Fertil Preservat Lab, Guangzhou, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
LIMK1/2; actin; embryo development; blastocyst; PORCINE OOCYTE MATURATION; LIM-KINASE; COFILIN PHOSPHORYLATION; EARLY COMPACTION; DYNAMICS; CELL; FERTILIZATION; CYTOSKELETON; ADF/COFILIN; BLASTOCYST;
D O I
10.1080/15384101.2018.1482138
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
LIMKs (LIMK1 and LIMK2) are serine/threonine protein kinases that involve in various cellular activities such as cell migration, morphogenesis and cytokinesis. However, its roles during mammalian early embryo development are still unclear. In the present study, we disrupted LIMK1/2 activity to explore the functions of LIMK1/2 during mouse early embryo development. We found that p-LIMK1/2 mainly located at the cortex of each blastomeres from 2-cell to 8-cell stage, and p-LIMK1/2 also expressed at morula and blastocyst stage in mouse embryos. Inhibition of LIMK1/2 activity by LIMKi 3 (BMS-5) at the zygote stage caused the failure of embryo early cleavage, and the disruption of LIMK1/2 activity at 8-cell stage caused the defects of embryo compaction and blastocyst formation. Fluorescence staining and intensity analysis results demonstrated that the inhibition of LIMK1/2 activity caused aberrant cortex actin expression and the decrease of phosphorylated cofilin in mouse embryos. Taken together, we identified LIMK1/2 as an important regulator for cofilin phosphorylation and actin assembly during mouse early embryo development.
引用
收藏
页码:1381 / 1389
页数:9
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