Reproduction Abstracts

Introduction: Multi-subunit protein complexes, called condensin I and condensin II, play a pivotal role in construction and segregation of mitotic chromosomes in many organisms. In mammals, however, previous studies examining condensins’ function are limited to siRNA-mediated knockdown experiments using some established cell lines. Hence the roles of both condensins in mammalian development have remained to be solved. In the present study, we have investigated defective phenotypes of knockout (KO) of Smc2, one of the core subunits for both condensins I and II, during mouse early embryogenesis.

Materials and methods: Heterozygous Smc2 KO mice were mated, and fertilized eggs were collected from the oviducts and cultured in vitro for 4 days. The embryos were fixed, immunofluorescently labeled with various antibodies, and observed with a confocal microscope.

Results and discussion: We found that SMC2 is essential for mammalian embryogenesis since no homozygous Smc2 KO mice were born. SMC2-deficient embryos showed a slight developmental delay after 4-day culture. In the embryos, the mitotic index was significantly higher than that in control embryos. Furthermore, all mitotic cells in SMC2-deficient embryos exhibited a variety of chromosomal defects: chromosome individualization, sister chromatid resolution, centromere organization and chromosome segregation were impaired. These results strongly suggest that condensins are essential for proper formation and segregation of chromosomes in mouse early embryos. Notably, we also noticed that heterochromatin organization in interphase nuclei was disordered in the SMC2-deficient embryos, implying that condensins might regulate chromatin architecture not only in M phase but also in interphase.