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Geminin deletion in mouse oocytes results in impaired embryo development and reduced fertility.

Molecular biology of the cell (2016-01-15)
Xue-Shan Ma, Fei Lin, Zhong-Wei Wang, Meng-Wen Hu, Lin Huang, Tie-Gang Meng, Zong-Zhe Jiang, Heide Schatten, Zhen-Bo Wang, Qing-Yuan Sun
ABSTRACT

Geminin controls proper centrosome duplication, cell division, and differentiation. We investigated the function of geminin in oogenesis, fertilization, and early embryo development by deleting the geminin gene in oocytes from the primordial follicle stage. Oocyte-specific disruption of geminin results in low fertility in mice. Even though there was no evident anomaly of oogenesis, oocyte meiotic maturation, natural ovulation, or fertilization, early embryo development and implantation were impaired. The fertilized eggs derived from mutant mice showed developmental delay, and many were blocked at the late zygote stage. Cdt1 protein was decreased, whereas Chk1 and H2AX phosphorylation was increased, in fertilized eggs after geminin depletion. Our results suggest that disruption of maternal geminin may decrease Cdt1 expression and cause DNA rereplication, which then activates the cell cycle checkpoint and DNA damage repair and thus impairs early embryo development.

MATERIALS
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Brand
Product Description

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Anti-BrdU antibody, Mouse monoclonal, clone BU-33, purified from hybridoma cell culture
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Anti-α-Tubulin−FITC antibody, Mouse monoclonal, clone DM1A, purified from hybridoma cell culture
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Anti-CDT1 Antibody, serum, from rabbit

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