CXCL12 and its receptor CXCR4 have well known roles in bone marrow homing and mobilization of hematopoietic stem cells and neutrophils, but inflammatory neutrophil recruitment is governed by CXCR2 and its chemokine ligands. However, researchers in Padova and Paris (Vargas lab discovered an important new role for CXCL12 helping neutrophils squeeze between endothelial cells when entering or exiting a blood vessel. The cell nucleus is the stiffest organelle, and CXCL12 activation of ACKR3 promotes nuclear plasticity and enhances neutrophil migration in spatially restricted environments. This previously unknown function of CXCL12 induces chromatin compaction by increasing lysine methylation on histone 4. These new results from the research groups of Antonella Viola and Pablo Vargas, recently published in Science Signaling, provide an exciting new link between chemokine signaling, heterochromatin abundance and nuclear morphology in migrating cells.

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Figure legend text: The chemokine CXCL12 increases the deformability of the nuclei in mouse neutrophils and compacts chromatin, enabling them to navigate narrow microchannels

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