This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Oh, S.
Right arrow Articles by Lim, D.-S.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Oh, S.
Right arrow Articles by Lim, D.-S.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, December 2009, p. 6309-6320, Vol. 29, No. 23
0270-7306/09/$08.00+0     doi:10.1128/MCB.00551-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Crucial Role for Mst1 and Mst2 Kinases in Early Embryonic Development of the Mouse{triangledown}

Sangphil Oh,1,{dagger} Dongjun Lee,1,{dagger} Tackhoon Kim,1,{dagger} Tae-Shin Kim,1 Hyun Jung Oh,1 Chae Young Hwang,2 Young-Yun Kong,3 Ki-Sun Kwon,2 and Dae-Sik Lim1*

National Research Laboratory of Molecular Genetics, Department of Biological Science, KAIST, Daejeon 305-701, South Korea,1 Laboratory of Cell Signaling, Aging Research Center, South Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, South Korea,2 Department of Biological Sciences, Seoul National University, San 56-1, Silim-dong, Gwanak-gu, Seoul 151-747, South Korea3

Received 28 April 2009/ Returned for modification 6 July 2009/ Accepted 31 August 2009

Mammalian sterile 20-like kinases 1 and 2 (Mst1 and Mst2, respectively) are potent serine/threonine kinases that are involved in cell proliferation and cell death. To investigate the physiological functions of Mst1 and Mst2, we generated Mst1 and Mst2 mutant mice. Mst1–/– and Mst2–/– mice were viable and fertile and developed normally, suggesting possible functional overlaps between the two genes. A characterization of heterozygous and homozygous combinations of Mst1 and Mst2 mutant mice showed that mice containing a single copy of either gene underwent normal organ development; however, Mst1–/–; Mst2–/– mice lacking both Mst1 and Mst2 genes started dying in utero at approximately embryonic day 8.5. Mst1–/–; Mst2–/– mice exhibited severe growth retardation, failed placental development, impaired yolk sac/embryo vascular patterning and primitive hematopoiesis, increased apoptosis in placentas and embryos, and disorganized proliferating cells in the embryo proper. These findings indicate that both Mst1 and Mst2 kinases play essential roles in early mouse development, regulating placental development, vascular patterning, primitive hematopoiesis, and cell proliferation and survival.

* Corresponding author. Mailing address: Department of Biological Sciences, Biomedical Research Center, South Korea Advanced Institute of Science and Technology, 373-1 Guseoung-dong, Yuseong-gu, Daejeon 305-701, South Korea. Phone: 82-42-350-2635. Fax: 82-42-350-2610. E-mail: daesiklim{at}kaist.ac.kr

{triangledown} Published ahead of print on 28 September 2009.

{dagger} These authors contributed equally to this work.

Molecular and Cellular Biology, December 2009, p. 6309-6320, Vol. 29, No. 23
0270-7306/09/$08.00+0     doi:10.1128/MCB.00551-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»