This Article Accepted Manuscript (PDF) All Versions of this Article: 137/6/931    most recent REP-09-0011v1 Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Maciejewska, Z. Articles by Ciemerych, M. Search for Related Content PubMed PubMed Citation Articles by Maciejewska, Z. Articles by Ciemerych, M.

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

Z Maciejewska, Faculty of Biology, Institute of Zoology, Department of Embryology, University of Warsaw, Warsaw, Poland
Z Polanski, Dept. Genetics & Evolution, Jagiellonian University, Institute of Zoology, Krakow, Poland
K Kisiel, Faculty of Biology, Animal Facility, University of Warsaw, Warsaw, Poland
J Kubiak, Institute of Genetics and Development, UMR 6061 CNRS/ University of Rennes, Rennes, France
M Ciemerych, Faculty of Biology, Institute of Zoology, Department of Cytology, University of Warsaw, Warsaw, Poland

Correspondence: Maria Ciemerych, Email: ciemerych{at}biol.uw.edu.pl

Abstract

The phenotype of 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 spindle assembly checkpoint 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 the preimplantation development and significantly decrease the reproductive success of this strain of mice. Thus, the common for meiosis and mitosis spindle assembly checkpoint - related failure participates in a complex LT/Sv phenotype.