Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 13, Issue 12, Pages 4470-4483Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E02-04-0241
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- NIGMS NIH HHS [GM-34770, R01 GM034770] Funding Source: Medline
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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 before stimulation caused 10% of the cells to lose their polarity by extending two opposing lateral lamellipodia. These multipolar 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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