Chemotaxis is the movement which carried out certain cells in response to a
chemical stimulus. In multicellular organisms, key cells are capable chemotactic
leukocytes. This ability is essential for immune system function and homeostasis
and its deregulation is associated with chronic inflammatory processes.

The movement of leukocytes is the result of an asymmetric
reorganization of their cytoskeleton: At the anterior end, the leading edge
expands due to polymerization of actin-F, while in the uropod retracts back
because of the contraction of actomyosin filaments. This reorganization is
asymmetric, in turn, result in the polarization of different molecules and the
complex signaling cascades that occur in response to chemical stimulation.
Santos Manes’s team at the National Center of Biotechnology, CSIC has conducted
various studies on the molecular mechanisms that cause this cell polarity. On
this occasion, have investigated the role of the enzyme phosphatidylinositol
4-phosphate 5-kinase type I isoform β (PIPKIβ) in HL60 neutrophil migration.

In polarized neutrophils by treatment with chemoattractant, the PIPKIβ
concentrates on uropods. To produce this distribution, PIPKIβ requires its
C-terminal domain specific to the β isoform. Overexpression of a modified form
of PIPKIβ which was deleted domain alters the chemotactic capacity of
neutrophils. This anomaly is associated with a failure in the polarization of
RhoA, monomeric G protein that in the normal chemotactic response, focuses on
the uropods which controls the contraction of actomyosin. A similar phenotype is
obtained by reducing the role of PIPKIβ by RNAi. In conclusion, Manes and
colleagues propose to PIPKIβ as a new element in the complex signaling network
that the identity of uropod in leukocytes.