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Spatial organization of differently fated cells within an organ is essential and needs to be maintained during development. This is largely implemented via compartment boundaries that serve as barriers between distinct cell types. Biased accumulation of junctional non-muscle Myosin II along the interface between differently fated groups of cells contributes to boundary integrity and maintains its shape via increased tension [1-4]. Here we test whether interfacial Myosin driven tension is responsible for the elimination of aberrantly specified cells that would otherwise compromise compartment organization. To this end, we genetically reduce Myosin II levels in three different patterns: in both wild-type and misspecified cells, only in misspecified cells and specifically at the interface between wild-type and aberrantly specified cells. We find that recognition and elimination of aberrantly specified cells do not rely on tensile forces driven by interfacial Myosin cables. Moreover, apical constriction of misspecified cells and their separation from wild type neighbors occurs even when Myosin level is greatly reduced. Thus, we conclude that the forces that drive elimination of aberrantly specified cells are largely independent of Myosin II. |
