a single bivalent efficiently inhibits cyclin b1 degradation and polar body extrusion in mouse oocytes indicating robust sac during female meiosis i一个二价有效地抑制细胞周期蛋白b1退化和极体挤压在小鼠卵母细胞显示强劲的囊在减数第一次分裂的女性.pdfVIP

a single bivalent efficiently inhibits cyclin b1 degradation and polar body extrusion in mouse oocytes indicating robust sac during female meiosis i一个二价有效地抑制细胞周期蛋白b1退化和极体挤压在小鼠卵母细胞显示强劲的囊在减数第一次分裂的女性.pdf

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a single bivalent efficiently inhibits cyclin b1 degradation and polar body extrusion in mouse oocytes indicating robust sac during female meiosis i一个二价有效地抑制细胞周期蛋白b1退化和极体挤压在小鼠卵母细胞显示强劲的囊在减数第一次分裂的女性

A Single Bivalent Efficiently Inhibits Cyclin B1 Degradation and Polar Body Extrusion in Mouse Oocytes Indicating Robust SAC during Female Meiosis I 1 2 2 1,3 Steffen Hoffmann , Bernard Maro , Jacek Z. Kubiak *, Zbigniew Polanski * 1 Department of Developmental Biology, Max Planck Institute of Immunobiology, Freiburg, Germany, 2 UMR 6061 CNRS/ University of Rennes 1, Mitosis Meiosis Group, IFR 140 GFAS, Rennes, France, 3 Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Cracow, Poland Abstract The Spindle Assembly Checkpoint (SAC) inhibits anaphase until microtubule-to-kinetochore attachments are formed, thus securing correct chromosome separation and preventing aneuploidy. Whereas in mitosis even a single unattached chromosome keeps the SAC active, the high incidence of aneuploidy related to maternal meiotic errors raises a concern about the lower efficiency of SAC in oocytes. Recently it was suggested that in mouse oocytes, contrary to somatic cells, not a single chromosome but a critical mass of chromosomes triggers efficient SAC pointing to the necessity of evaluating the robustness of SAC in oocytes. Two types of errors in chromosome segregation upon meiosis I related to SAC were envisaged: (1) SAC escape, when kinetochores emit SAC-activating signal unable to stop anaphase I; and (2) SAC deceive, when kinetochores do not emit the signal. Using micromanipulations and live imaging of the first polar body extrusion, as well as the dynamics of cyclin B1 degradation, here we show that in mouse oocytes a single bivalent keeps the SAC active. This is the first direct evaluation of SAC efficiency in mouse oocytes, which provides strong evidence that

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