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Publication : Targeted disruption of Mcm10 causes defective embryonic cell proliferation and early embryo lethality.

First Author  Lim HJ Year  2011
Journal  Biochim Biophys Acta Volume  1813
Issue  10 Pages  1777-83
PubMed ID  21693137 Mgi Jnum  J:177618
Mgi Id  MGI:5295554 Doi  10.1016/j.bbamcr.2011.05.012
Citation  Lim HJ, et al. (2011) Targeted disruption of Mcm10 causes defective embryonic cell proliferation and early embryo lethality. Biochim Biophys Acta 1813(10):1777-83
abstractText  Minichromosome maintenance 10 (MCM10) is a conserved, abundant nuclear protein, which plays a key role in the initiation of eukaryotic chromosomal DNA replication and elongation. To elucidate the physiological importance of MCM10 in vivo, we generated conventional knockout mice. No MCM10-null embryos were recovered after E8.5, and the mutation was found to be lethal before the implantation stage. Mutant embryos showed apparently normal growth until the morula stage, but growth defects after this stage. The dramatic reduction of 5-bromo-2-deoxyuridine (BrdU) incorporation in the mutant embryo, followed by cell death, suggests that defective cell proliferation may underlie this developmental failure. Taken together, these findings provide the first unequivocal genetic evidence for an essential and non-redundant physiological role of MCM10 during murine peri-implantation development.
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