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Polo‐like kinase 1 may regulate G2/M transition of mouse fertilized eggs by means of inhibiting the phosphorylation of Tyr15 of Cdc2
Author(s) -
Zhang Zhe,
Su Wenhui,
Feng Chen,
Yu Dahai,
Cui Cheng,
Xu Xiaoyan,
Yu Bingzhi
Publication year - 2007
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.20703
Subject(s) - biology , plk1 , cyclin dependent kinase 1 , kinase , phosphorylation , mitosis , microbiology and biotechnology , polo like kinase , protein kinase a , cell cycle , cell , biochemistry
Abstract Polo‐like kinase 1(Plk1) has been reported to be a multifunctional kinase that plays pivotal regulatory roles in microtubule assembly during mammalian early embryonic mitosis. In the present study, we examined the expression of Plk1 at protein and mRNA level in mouse fertilized eggs by Western blot and RT‐PCR. We also examined the kinase activity of Plk1. At various developmental phases of mouse one‐cell stage embryos, both the protein and the mRNA of Plk1 were uniformly distributed; but the kinase activity of Plk1 increased at G2/M phase and decreased at the end of M phase. At the meantime, the phosphorylation of Tyr15 of Cdc2 was inhibited at M phase. To investigate its function in mammalian fertilized eggs further, we used specific short hairpin RNAs (shRNA) and scytonemin, the putative inhibitor of Plk1 to suppress the activity of Plk1 in mouse fertilized eggs. Upon blockage of the activation of with Plk1 shRNA and scytonemin in mouse one‐cell stage embryos, the cleavage rate decreased and the phosphorylation level of Tyr15 of Cdc2 increased. These results imply that the Plk1 may regulate cell cycle progression of mouse fertilized eggs by means of inhibiting the phosphorylation of Tyr15 of Cdc2. Mol. Reprod. Dev. 74: 1247–1254, 2007. © 2007 Wiley‐Liss, Inc.