Spindle Assembly Checkpoint Regulates Mitotic Cell Cycle Progression during Preimplantation Embryo DevelopmentReport as inadecuate




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Errors in chromosome segregation or distribution may result in aneuploid embryo formation, which causes implantation failure, spontaneous abortion, genetic diseases, or embryo death. Embryonic aneuploidy occurs when chromosome aberrations are present in gametes or early embryos. To date, it is still unclear whether the spindle assembly checkpoint SAC is required for the regulation of mitotic cell cycle progression to ensure mitotic fidelity during preimplantation development. In this study, using overexpression and RNA interference RNAi approaches, we analyzed the role of SAC components Bub3, BubR1 and Mad2 in mouse preimplantation embryos. Our data showed that overexpressed SAC components inhibited metaphase-anaphase transition by preventing sister chromatid segregation. Deletion of SAC components by RNAi accelerated the metaphase-anaphase transition during the first cleavage and caused micronuclei formation, chromosome misalignment and aneuploidy, which caused decreased implantation and delayed development. Furthermore, in the presence of the spindle-depolymerizing drug nocodazole, SAC depleted embryos failed to arrest at metaphase. Our results suggest that SAC is essential for the regulation of mitotic cell cycle progression in cleavage stage mouse embryos.



Author: Yanchang Wei, Saima Multi, Cai-Rong Yang, Junyu Ma, Qing-Hua Zhang, Zhen-Bo Wang, Mo Li, Liang Wei, Zhao-Jia Ge, Chun-Hui Zhang,

Source: http://plos.srce.hr/



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