Fig. 8

Model. a Schematic representation of the phenotypes observed in control conditions, after depletion of Msn or in Msn-depleted clusters expressing Moe^T556D or Rok^CAT. Phenotypes were scored on a scale of 0 to 1, where 0 is the wild-type phenotype and 1 stands for a strong defects observed after Msn depletion. We categorized each readout into four main categories being Protrusion restriction, Cortical tension, Cell contractility, and Cell Motility. Active Moe (Moe^T556D) rescues parameters associated with cell communication and partially rescues Msn depletion-induced cell shape defects. Conversely, Rok^CAT expression rescues cell contractility and partially restores cell motility but not cell communication. b Working model. The kinase Misshapen regulates cortical stiffness and protrusion restriction by directly phosphorylating Moesin. Independently, Misshapen regulates cluster detachment and dynamics through acto-myosin contractility regulation