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Furthermore, deregulation of their functions is deleterious to tissue architecture and can result in the sorting of somatic rounded clones minimizing their contact with surrounding wild-type (wt) cells. Defects in somatic clones shape correlate with defects in proliferation, cell affinity, cell-cell adhesion, oriented cell division and cortical elasticity. Combining genetics, live-imaging, laser ablation and computer simulations, we aim to analyze whether distinct or similar mechanisms can account for the common role of tumor-suppressor and proto-oncogenes in cell-cell contact regulation. In Drosophila epithelia, Fat (Ft) and Dachsous (Ds) tumor-suppressors regulate cell proliferation, tissue morphogenesis, planar cell polarity and junction tension. By analyzing the time evolution of ft mutant cells and clones, we show that ft clones reduce their cell-cell contact with surrounding wt tissue in the absence of concomitant cell divisions and over-proliferation. This contact reduction depends on opposite changes of junction tensions in the clone bulk and its boundary with neighboring wt tissue. More generally, either clone bulk or boundary junction tensions is modulated by the activation of Yorkie, Myc and Ras yielding similar contact reductions with wt cells. 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