During Drosophila oogenesis, interactions between somatic cells and germline cells are crucial for oocyte polarisation and the subsequent formation of the body axes, but the molecular nature of the signals that regulate these interactions is not known. Here, on p. 1991, Trudi Schüpbach and co-workers show that, by regulating myosin activity, protein phosphatase 1β (PP1β) in the posterior follicle cells (PFCs) of Drosophila ovaries controls the generation of an oocyte polarising signal. The researchers first identified a loss-of-function mutation of flapwing, which encodes the catalytic subunit of PP1β, that disrupts oocyte polarisation. They show that excessive mysosin activity in PFCs caused by PP1β disruption leads to defective PFC Notch signalling and endocytosis. This sensitivity to defective Notch signalling, they report, requires JAK/STAT and EGFR signalling in the PFCs. Importantly, the researchers also identify a Notch-independent role for myosin activity in controlling oocyte polarisation, highlighting an additional link between the mechanical force-generating machinery of the cell and the ooctye polarisation pathway.