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Collective cell migration is a highly complex process in which groups of cells move together. A fundamental question is how cell ensembles can migrate efficiently. In some cases, the group is no more than a collection of individual cells. In others, the group behaves as a supracellular unit, whereby the cell group could be considered as a giant 'supracell', the concept of which was conceived over a century ago. The development of recent tools has provided considerable evidence that cell collectives are highly cooperative, and their migration can better be understood at the tissue level, rather than at the cell level. In this Review, we will define supracellular migration as a type of collective cell migration that operates at a scale higher than the individual cells. We will discuss key concepts of supracellular migration, review recent evidence of collectives exhibiting supracellular features and argue that many seemingly complex collective movements could be better explained by considering the participating cells as supracellular entities. [ABSTRACT FROM AUTHOR]

Cell migration is an essential and highly regulated process. During development, glia cells and neurons migrate over long distances -- in most cases collectively -- to reach their final destination and build the sophisticated architecture of the nervous system, the most complex tissue of the body. Collective migration is highly stereotyped and efficient, defects in the process leading to severe human diseases that include mental retardation. This dynamic process entails extensive cell communication and coordination, hence, the real challenge is to analyze it in the entire organism and at cellular resolution. We here investigate the impact of the N-cadherin adhesion molecule on collective glial migration, by using the Drosophila developing wing and cell-type specific manipulation of gene expression. We show that N-cadherin timely accumulates in glial cells and that its levels affect migration efficiency. N-cadherin works as a molecular brake in a dosage-dependent manner, by negatively controlling actin nucleation and cytoskeleton remodeling through a/p catenins. This is the first in vivo evidence for N-cadherin negatively and cell autonomously controlling collective migration. [ABSTRACT FROM AUTHOR]

Collective cell migration is absolutely essential for a wide variety of physiological episodes including the re-epithelialisation component of tissue repair. However, the investigation of such processes has been frustrated by difficulties in quantitatively analysing the behaviours of a large body of cells within a migrating epithelial sheet, which previously required manually tracking a large number of individual cells, or using advanced computational techniques. Here, we describe a novel and simpler image subtraction method with which we can visualise and quantify collective cell mobilisation as a 'white wave' that propagates back from the leading edge of a scratch-wounded monolayer of cultured epithelial cells. Using this technique, we show that actomyosin constriction negatively regulates cell mobilisation and that the advancement of cell sheets and the mobilisation of rows of cells behind their leading edges are independently regulated. We also show that there is a finite limit to the number of rows of cells mobilised after wounding. Moreover, our data suggest that enhancing cell mobilisation, by release from myosin II contractility, accelerates the healing of large wounds in the long term, thus raising the possibility that the cell mobilisation 'wave' we reveal here might be a therapeutic target for improving wound healing. [ABSTRACT FROM AUTHOR]

Collective migration is a key feature of the social amoebae Dictyostelium discoideum, where the binding of chemoattractants leads to the production and secretion of additional chemoattractant and the relay of the signal to neighboring cells. This then guides cells to migrate collectively in a head-to-tail fashion. We used mutants that were defective in signal relay to elucidate which quantitative metrics of cell migration are most strongly affected by signal relay and collective motion. We show that neither signal relay nor collective motion markedly impact the speed of cell migration. Cells maintained a preferred overall direction of motion for several minutes with similar persistence, regardless of whether or not they were attracted to moving neighbors, moving collectively in contact with their neighbors, or simply following a fixed exogenous signal. We quantitatively establish that signal relay not only increases the number of cells that respond to a chemotactic signal, but most remarkably, also transmits information about the location of the source accurately over large distances, independently of the strength of the exogenous signal. We envision that signal relay has a similar key role in the migration of a variety of chemotaxing mammalian cells that can relay chemoattractant signals. [ABSTRACT FROM AUTHOR]

Collective cell migration is a key process during the development of most organisms. It can involve either the migration of closely packed mesenchymal cells that make dynamic contacts with frequently changing neighbour cells, or the migration of epithelial sheets that typically display more stable cell-cell interactions and less frequent changes in neighbours. These collective movements can be controlled by short- or long-range dynamic gradients of extracellular signalling molecules, depending on the number of cells involved and their distance of migration. These gradients are sensed by some or all of the migrating cells and translated into directed migration, which in many settings is further modulated by cell-contact-mediated attractive or repulsive interactions that result in contact-following or contact-inhibition of locomotion, respectively. Studies of collective migration of groups of epithelial cells during development indicate that, in some cases, only leader cells sense and migrate up an external signal gradient, and that adjacent cells follow through strong cell-cell contacts. In this Commentary, I review studies of collective cell migration of differently sized cell populations during the development of several model organisms, and discuss our current understanding of the molecular mechanisms that coordinate this migration. [ABSTRACT FROM AUTHOR]