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During animal development, proliferating tissues are subdivided into compartments, which prevent cells with different identities from mixing. The segregation of cell populations at compartment boundaries defines cell lineages and is crucial for the correct patterning and differentiation of tissues. Although this organizing principle is conserved from flies to humans, the mechanisms that separate cells at boundaries remain unclear. Two groups now report that cell sorting is directed by mechanical tension along the boundaries, and that this tension depends on actomyosin contractility.

Landsberg et al. analysed the role of mechanical tension in sorting cells at the anteroposterior compartment boundary in developing Drosophila melanogaster wings. The boundary is defined by apical adherens junctions between adjacent cells at the border of the anterior and posterior compartments, which are enriched in filamentous (F)-actin and non-muscle myosin II (NM II). Using an ultraviolet laser beam focused on the plane of apical adherens junctions, the authors cut single apical adherens junctions and measured the velocity and the extent of cell corner–corner separation, which is a measure of the physical tension at cell–cell bonds. This tension is increased 2.5-fold along the anteroposterior boundary in comparison with the remaining tissue. Importantly, by integrating these measurements into a mathematical model that simulates the growth of two adjacent proliferating cell populations, the authors show that a 2.5-fold increase in bond tension, which they suggest might be dependent on actomyosin filament (made of bipolar NM II filaments and F-actin, which interact to exert tension) contractility, is sufficient to maintain a compartment boundary.

Monier et al. investigated how cells are stopped from invading neighbouring compartments in D. melanogaster early embryo trunks, which are divided into alternating anterior and posterior compartments. The anteroposterior boundary is enriched in NM II and F-actin, which form a linear actomyosin cable-like structure. Cells on each side of the boundary contribute to the actomyosin cable, which localizes at apical adherens junctions. Whole-embryo inhibition of NM II induces cell-sorting defects, suggesting that the apical actomyosin cable prevents cell mixing at compartmental boundaries. In untreated dividing cells, the cable deforms but then straightens back, and daughter cells return to their compartment of origin. The authors show that chromophore-assisted laser inactivation (CALI) can be used to inhibit NM II fused to green fluorescent protein with subcellular resolution in live embryos. Inactivating NM II at the cable with CALI in dividing cells leads to an irregular boundary and cell mixing, showing that this structure is necessary for cell sorting.

Together, these studies show that regulation of actomyosin-dependent cortical tension might be the primary mechanism to maintain boundaries in proliferating tissues.

Author: Kim Baumann - Copyright © 2010 Nature Publishing Group, a division of MacMillan Publishers Limited; used with permission