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Spindle assembly checkpoint-related failure perturbs early embryonic divisions and reduces reproductive performance of LT/Sv mice

Departments of¹ , Embryology² Cytology, Institute of Zoology, Faculty of Biology, University of Warsaw, Ilji Miecznikowa 1, 02-096 Warsaw, Poland³ Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Ingardena 6, 30-060 Cracow, Poland⁴ Department of Developmental Biology, Max Planck Institute of Immunobiology, Freiburg D-79108, Germany⁵ Animal Facility, Faculty of Biology, University of Warsaw, Warsaw, Poland⁶ ‘Mitosis and Meiosis’ Group, Institute of Genetics and Development, University of Rennes 1, CNRS-UMR 6061, IFR 140 GFAS, 35043 Rennes, France

Correspondence should be addressed to M A Ciemerych; Email: ciemerych{at}biol.uw.edu.pl J Z Kubiak; Email: jacek.kubiak{at}univ-rennes1.fr

Z Maciejewska is now at Molecular Basis of Carcinogenesis, Institut de Recherche sur le Cancer de Montpellier, Montpellier, France

The phenotype of the LT/Sv strain of mice is manifested by abnormalities in oocyte meiotic cell-cycle, spontaneous parthenogenetic activation, teratomas formation, and frequent occurrence of embryonic triploidy. These abnormalities lead to the low rate of reproductive success. Recently, metaphase I arrest of LT/Sv oocytes has been attributed to the inability to timely inactivate the spindle assembly checkpoint (SAC). As differences in meiotic and mitotic SAC functioning were described, it remains obscure whether this abnormality is limited to the meiosis or also impinges on the mitotic divisions of LT/Sv embryos. Here, we show that a failure to inactivate SAC affects mitoses during preimplantation development of LT/Sv embryos. This is manifested by the prolonged localization of MAD2L1 on kinetochores of mitotic chromosomes and abnormally lengthened early embryonic M-phases. Moreover, LT/Sv embryos exhibit elevated frequency of abnormal chromosome separation during the first mitotic division. These abnormalities participate in severe impairment of preimplantation development and significantly decrease the reproductive success of this strain of mice. Thus, the common meiosis and mitosis SAC-related failure participates in a complex LT/Sv phenotype.