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Molecular Endocrinology Vol. 3, No. 3 588-596
doi:10.1210/mend-3-3-588
Copyright © 1989 by the Endocrine Society.
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The Presence of Parvalbumin in a Nonmuscle Cell Line Attenuates Progression through Mitosis

Colin D. Rasmussen and Anthony R. Means

Department of Cell Biology, Baylor College of Medicine Houston, Texas 77030

Address requests for reprints to: Dr. Colin D. Rasmussen, Department of Cell Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, Texas 77030.

Abstract

Based on studies that have examined the effect of calcium chelators on cells, it has been proposed that this cation plays a role in regulating cell proliferation. In this study a novel approach was used to indirectly examine the role of calcium in cell cycle progression. A cDNA for the Ca2+-binding protein parvalbumin has been expressed in mouse C127 cells, using a bovine papilloma virus-based expression vector. The normal role of parvalbumin is that of a calcium buffer in vertebrate fast twitch muscle, and the C127 cells do not normally express this protein. The presence of parvalbumin had several effects on the growth of C127 cells. The most striking phenotype was an increase in cell cycle duration which analysis showed was the result of an increase the length of d and mitosis (predominantly at prophase). Since changes in cell cycle duration typically occur as a result of changes in G1 duration, the observed increase in the length of mitosis is most unusual. The present results indicate that the previously observed increase in the rate of cell proliferation in cells with elevated calmodulin levels is not the result of a general increase in the level of cytoplasmic calciumbinding protein, but is specific to calmodulin. In addition, the results suggest that calcium regulates progression through mitosis by both calmodulin-dependent (metaphase transition) and -independent (prophase) mechanisms.

FOOTNOTES

This work was supported by Grant BC-326 from the American Cancer Society.

Received for publication November 7, 1988. Revision received December 7, 1988. Accepted for publication December 7, 1988.




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Copyright © 1989 by The Endocrine Society