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Originally published online as doi:10.1189/jlb.1001894 on May 22, 2003

Published online before print May 22, 2003
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(Journal of Leukocyte Biology. 2003;73:830-840.)
© 2003 by Society for Leukocyte Biology

Role of Rho-family GTPase Cdc42 in polarized expression of lymphocyte appendages

Stuart Ratner*,{dagger}, Marie P. Piechocki* and Anne Galy{ddagger}

* Breast Cancer Research Program and
{ddagger} Stem Cell Transplantation Program, Barbara Ann Karmanos Cancer Institute, and
{dagger} Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, Michigan

Correspondence: Dr. Stuart Ratner, Breast Cancer Research Program, Barbara Ann Karmanos Cancer Institute, 110 E. Warren Ave., Detroit, MI 48201. E-mail: ratners{at}kci.wayne.edu

Lymphocytes polarize for motility by developing a broad anterior, where lamellipodia arise, and a simple stalk-like posterior appendage, the uropod. Through time-lapse analysis of normal and leukemic human T cells, it was found that this polarized form is maintained by a mechanism that excludes lamellipodia from the uropod. Lamellipodia regularly traveled rearward to encroach upon the uropod but disassembled abruptly at the uropod border. This exclusion of lamellipodia from the uropod required the Rho-family guanosine triphosphatase Cdc42. Reduction of Cdc42 activity by expression of dominant-negative Cdc42 resulted in "two headed" cells in which lamellipodia persisted at the distal end of the uropod. Random and chemotactic motility were impaired. Increased Cdc42 activity, induced by expression of activated, mutant Cdc42, was accompanied by a general loss of lamellipodia. The results suggest that one role of Cdc42 in lymphocyte motility is to preserve polarity by concentrating lamellipodial disassembly signals in the uropod.

Key Words: human • T cell • leukemia • motility • chemotaxis • cytoskeleton




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