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Molecular and Cellular Biology, November 2001, p. 7183-7190, Vol. 21, No. 21
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.21.7183-7190.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

MEKK1 Is Essential for DT40 Cell Apoptosis in Response to Microtubule Disruption

Raymond Kwan,1 Joan Burnside,2 Tomohiro Kurosaki,3 and Genhong Cheng1,4,*

Molecular Biology Institute1 and Department of Microbiology, Immunology and Molecular Genetics, Jonsson Comprehensive Cancer Center,4 University of California Los Angeles, Los Angeles, California 90095-1781; Department of Animal and Food Sciences, College of Agriculture and Natural Resources, University of Delaware, Newark, Delaware 19717-13032; and Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570-8506, Japan3

Received 27 March 2001/Returned for modification 23 May 2001/Accepted 10 August 2001

Vinblastine and other microtubule-damaging agents, such as nocodazole and paclitaxel, cause cell cycle arrest at the G2/M transition and promote apoptosis in eukaryotic cells. The roles of these drugs in disrupting microtubule dynamics and causing cell cycle arrest are well characterized. However, the mechanisms by which these agents promote apoptosis are poorly understood. We disrupted the MEKK1 kinase domain in chicken bursal B-cell line DT40 by homologous recombination and have shown that it is essential for both vinblastine-mediated apoptosis and vinblastine-mediated c-Jun N-terminal protein kinase activation. In addition, our data indicate that vinblastine-mediated apoptosis in DT40 cells requires new protein synthesis but does not require G2/M arrest, suggesting that vinblastine-mediated cell cycle arrest and apoptosis are two independent processes.

* Corresponding author. Mailing address: Department of Microbiology, Immunology & Molecular Genetics, 8-240J Factor, UCLA, Los Angeles, CA 90095-1781. Phone: (310) 825-8896. Fax: (310) 206-5553. E-mail: genhongc{at}microbio.ucla.edu.

Molecular and Cellular Biology, November 2001, p. 7183-7190, Vol. 21, No. 21
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.21.7183-7190.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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