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Molecular and Cellular Biology, July 2006, p. 5373-5381, Vol. 26, No. 14
0270-7306/06/$08.00+0     doi:10.1128/MCB.00043-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Mouse emi1 Has an Essential Function in Mitotic Progression during Early Embryogenesis{dagger}

Ho Lee,1,2 Dong Jun Lee,1 Sang Phil Oh,1 Hee Dong Park,1 Hyun Hee Nam,3 Jin Man Kim,3 and Dae-Sik Lim1*

Department of Biological Sciences and Biomedical Research Center, Korea Advanced Institute of Science and Technology, 373-1 Guseoung-dong, Yuseong-gu, Daejeon 305-701, South Korea,1 National Cancer Center, 809 Madu1-dong, Ilsandon-gu, Goyang-si, Gyeonggi-do 410-769, South Korea,2 Department of Pathology, College of Medicine, Chungnam National University, 6 Munwha-dong Jung-gu, Daejeon 301-131, South Korea3

Received 9 January 2006/ Returned for modification 2 February 2006/ Accepted 28 April 2006

For successful mitotic entry and spindle assembly, mitosis-promoting factors are activated at the G2/M transition stage, followed by stimulation of the anaphase-promoting complex (APC), an E3 ubiquitin ligase, to direct the ordered destruction of several critical mitotic regulators. Given that inhibition of APC activity is important for preventing premature or improper ubiquitination and destruction of substrates, several modulators and their regulation mechanisms have been studied. Emi1, an early mitotic inhibitor, is one of these regulatory factors. Here we show, by analyzing Emi1-deficient embryos, that Emi1 is essential for precise mitotic progression during early embryogenesis. Emi1–/– embryos were found to be lethal due to a defect in preimplantation development. Cell proliferation appeared to be normal, but mitotic progression was severely defective during embryonic cleavage. Moreover, multipolar spindles and misaligned chromosomes were frequently observed in Emi1 mutant cells, possibly due to premature APC activation. Our results collectively suggest that the late prophase checkpoint function of Emi1 is essential for accurate mitotic progression and embryonic viability.

* Corresponding author. Mailing address: Department of Biological Sciences, Biomedical Research Center, Korea Advanced Institute of Science and Technology, 373-1 Guseoung-dong, Yuseong-gu, Daejeon 305-701, South Korea. Phone: 82-42-869-2635. Fax: 82-42-869-2610. E-mail: daesiklim{at}kaist.ac.kr.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, July 2006, p. 5373-5381, Vol. 26, No. 14
0270-7306/06/$08.00+0     doi:10.1128/MCB.00043-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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