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Type I phosphatidylinositol 4-phosphate 5-kinase controls neutrophil polarity and directional movement

AutorLacalle, Rosa Ana; Peregil, Rosa M.; Albar, Juan Pablo; Merino Plaza, Ernesto; Martínez-Alonso, Carlos; Mérida, Isabel; Mañes, Santos
Fecha de publicacióndic-2007
EditorRockefeller University Press
CitaciónThe Journal of Cell Biology, Vol. 179, No. 7, pp. 1539-1553
ResumenDirectional cell movement in response to external chemical gradients requires establishment of front–rear asymmetry, which distinguishes an up-gradient protrusive leading edge, where Rac-induced F-actin polymerization takes place, and a down-gradient retractile tail (uropod in leukocytes), where RhoA-mediated actomyosin contraction occurs. The signals that govern this spatial and functional asymmetry are not entirely understood. We show that the human type I phosphatidylinositol 4-phosphate 5-kinase isoform β (PIPKIβ) has a role in organizing signaling at the cell rear. We found that PIPKIβ polarized at the uropod of neutrophil-differentiated HL60 cells. PIPKIβ localization was independent of its lipid kinase activity, but required the 83 C-terminal amino acids, which are not homologous to other PIPKI isoforms. The PIPKIβ C terminus interacted with EBP50 (4.1-ezrin-radixin-moesin (ERM)-binding phosphoprotein 50), which enabled further interactions with ERM proteins and the Rho-GDP dissociation inhibitor (RhoGDI). Knockdown of PIPKIβ with siRNA inhibited cell polarization and impaired cell directionality during dHL60 chemotaxis, suggesting a role for PIPKIβ in these processes.
DescripciónCopyright by The Rockefeller University Press
URIhttp://hdl.handle.net/10261/3242
DOI10.1083/jcb.200705044
ISBN0021-9525
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