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A more recent version of this article appeared on December 1, 2002
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Submitted on May 1, 2002
Revised on July 18, 2002
Accepted on August 21, 2002
1 Department of Biochemistry, E-215, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021
* Corresponding author. E-mail address: frmaxfie{at}med.cornell.edu.
The development of cell polarity in response to chemoattractant stimulation in human polymorphonuclear neutrophils (PMNs) is characterized by the rapid conversion from round to polarized morphology with a leading lamellipod at the front and a uropod at the rear. During PMN polarization, the microtubule (MT) array undergoes a dramatic reorientation toward the uropod that is maintained during motility and does not require large-scale MT disassembly or cell adhesion to the substratum. MTs are excluded from the leading lamella during polarization and motility, but treatment with a myosin light chain kinase inhibitor (ML-7) or the actin-disrupting drug, cytochalasin D, causes an expansion of the MT array and penetration of MTs into the lamellipod. Depolymerization of the MT array prior to stimulation caused 10% of the cells to lose their polarity by extending two opposing lateral lamellipodia. These multi-polar cells showed altered localization of a leading lamella-specific marker, talin, and a uropod-specific marker, CD44. In summary, these results indicate that F-actin and myosin II-dependent forces lead to the development and maintenance of MT asymmetry that may act to reinforce cell polarity during PMN migration.
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