The collective migration of cells as a cohesive group is a hallmark of the tissue remodelling events that underlie embryonic morphogenesis, wound repair and cancer invasion. In such migration, cells move as sheets, strands, clusters or ducts rather than individually, and use similar actin- and myosin-mediated protrusions and guidance by extrinsic chemotactic and mechanical cues as used by single migratory cells. However, cadherin-based junctions between cells additionally maintain 'supracellular' properties, such as collective polarization, force generation, decision making and, eventually, complex tissue organization. Comparing different types of collective migration at the molecular and cellular level reveals a common mechanistic theme between developmental and cancer research.

/pdf/collective-cell-migration-in-morphogenesis-regeneration-and-21h8h3dmpy.pdf

Collective cell migration in morphogenesis, regeneration and cancer

Oogenesis in teleosts: How fish eggs are formed

https://www.cell.com/immunity/pdf/S1074-7613(12)00193-8.pdf

The Chemokine Superfamily Revisited

Sixteen years ago, the Nomenclature Committee of the International Union of Pharmacology approved a system for naming human seven-transmembrane (7TM) G protein-coupled chemokine receptors, the large family of leukocyte chemoattractant receptors that regulates immune system development and function, in large part by mediating leukocyte trafficking. This was announced in Pharmacological Reviews in a major overview of the first decade of research in this field [Murphy PM, Baggiolini M, Charo IF, Hebert CA, Horuk R, Matsushima K, Miller LH, Oppenheim JJ, and Power CA (2000) Pharmacol Rev 52:145–176]. Since then, several new receptors have been discovered, and major advances have been made for the others in many areas, including structural biology, signal transduction mechanisms, biology, and pharmacology. New and diverse roles have been identified in infection, immunity, inflammation, development, cancer, and other areas. The first two drugs acting at chemokine receptors have been approved by the U.S. Food and Drug Administration (FDA), maraviroc targeting CCR5 in human immunodeficiency virus (HIV)/AIDS, and plerixafor targeting CXCR4 for stem cell mobilization for transplantation in cancer, and other candidates are now undergoing pivotal clinical trials for diverse disease indications. In addition, a subfamily of atypical chemokine receptors has emerged that may signal through arrestins instead of G proteins to act as chemokine scavengers, and many microbial and invertebrate G protein-coupled chemokine receptors and soluble chemokine-binding proteins have been described. Here, we review this extended family of chemokine receptors and chemokine-binding proteins at the basic, translational, and clinical levels, including an update on drug development. We also introduce a new nomenclature for atypical chemokine receptors with the stem ACKR (atypical chemokine receptor) approved by the Nomenclature Committee of the International Union of Pharmacology and the Human Genome Nomenclature Committee.

https://pharmrev.aspetjournals.org/content/pharmrev/66/1/1.full.pdf

International Union of Pharmacology. LXXXIX. Update on the Extended Family of Chemokine Receptors and Introducing a New Nomenclature for Atypical Chemokine Receptors

Chemokines, small pro-inflammatory chemoattractant cytokines that bind to specific G-protein-coupled seven-span transmembrane receptors, are major regulators of cell trafficking and adhesion. The chemokine CXCL12 (also called stromal-derived factor-1) is an important α-chemokine that binds primarily to its cognate receptor CXCR4 and thus regulates the trafficking of normal and malignant cells. For many years, it was believed that CXCR4 was the only receptor for CXCL12. Yet, recent work has demonstrated that CXCL12 also binds to another seven-transmembrane span receptor called CXCR7. Our group and others have established critical roles for CXCR4 and CXCR7 on mediating tumor metastasis in several types of cancers, in addition to their contributions as biomarkers of tumor behavior as well as potential therapeutic targets. Here, we review the current concepts regarding the role of CXCL12 / CXCR4 / CXCR7 axis activation, which regulates the pattern of tumor growth and metastatic spread to organs expressing high levels of CXCL12 to develop secondary tumors. We also summarize recent therapeutic approaches to target these receptors and/or their ligands.

CXCL12 / CXCR4 / CXCR7 chemokine axis and cancer progression.

Control of Chemokine-Guided Cell Migration by Ligand Sequestration

Summary 24 hr of embryonic development (Weidinger et al., 1999, 2002). The migration route of the PGCs is prefigured by Zebrafish primordial germ cells (PGCs) are guided to- the dynamic expression pattern of the chemokine SDF-ward their targets by the chemokine SDF-1a. PGCs 1awhosereceptor,CXCR4b,isexpressedbythemigrat- were followed during three phases of their migration: ing cells (Doitsidou et al., 2002). Responding to the che-when migrating as individual cells, while remaining in motactic signals provided by SDF-1a, PGCs migrate in a clustered configuration, and when moving as a cell distinct steps during which they arrive at intermediatecluster within the embryo. We found that individually targets before reaching their final target (Weidinger et migrating PGCs alternate between migratory and al.,1999,2002).Incontrast,cellsinwhichCXCR4b/SDF-pausing modes. Pausing intervals are characterized 1a signaling is disrupted migrate nondirectionally and by loss of cell polarity and correlate with subsequent consequently are distributed throughout the embryochangesinthedirectionofmigration.Theseproperties

Short Article Autonomous Modes of Behavior in Primordial Germ Cell Migration

https://pure.mpg.de/pubman/item/item_598922_4/component/file_598921/230244.pdf

Autonomous modes of behavior in primordial germ cell migration.

Control of receptor internalization, signaling level, and precise arrival at the target in guided cell migration

The precise positioning of organ progenitor cells constitutes an essential, yet poorly understood step during organogenesis. Using primordial germ cells that participate in gonad formation, we present the developmental mechanisms maintaining a motile progenitor cell population at the site where the organ develops. Employing high-resolution live-cell microscopy, we find that repulsive cues coupled with physical barriers confine the cells to the correct bilateral positions. This analysis revealed that cell polarity changes on interaction with the physical barrier and that the establishment of compact clusters involves increased cell-cell interaction time. Using particle-based simulations, we demonstrate the role of reflecting barriers, from which cells turn away on contact, and the importance of proper cell-cell adhesion level for maintaining the tight cell clusters and their correct positioning at the target region. The combination of these developmental and cellular mechanisms prevents organ fusion, controls organ positioning and is thus critical for its proper function.

/pdf/repulsive-cues-combined-with-physical-barriers-and-cell-cell-4td58xtfhc.pdf

Sofia Minina

Papers

Control of Chemokine-Guided Cell Migration by Ligand Sequestration

Short Article Autonomous Modes of Behavior in Primordial Germ Cell Migration

Autonomous modes of behavior in primordial germ cell migration.

Control of receptor internalization, signaling level, and precise arrival at the target in guided cell migration

Repulsive cues combined with physical barriers and cell–cell adhesion determine progenitor cell positioning during organogenesis