Actomyosin flows are involved in a variety of cellular processes, including cytokinesis, cell migration, polarization, and morphogenesis. In epithelia, flow polarization orients cell deformations. It is unclear, however, how flows are polarized and how global patterns of junction remodeling emerge from flow polarization locally. We address this question during intercalation-driving extension of the Drosophila germband. Intercalation is associated with polarized junction remodeling, whereby actomyosin pulses flow anisotropically toward dorsal-ventral junctions and shrink them. Here, we show that planar polarization of flows emerges from polarized fluctuations in the levels of E-cadherin clusters that produce transient and oscillating asymmetries of coupling. These fluctuations are triggered by polarized E-cadherin endocytosis and are amplified by flow itself. This work suggests that fluctuations and mechanical instability are not the consequences of limited control over the systems key parameters, but rather that they define the axis of symmetry breaking.