In culture, cells typically lose their apicobasal polarity and their cell-cell interactions when they migrate. However, in vivo, collective cell migration is a common phenomenon, and apicobasal polarity is often at least partially maintained. How and why migrating cell clusters retain their apicobasal polarity is still poorly understood. The border cell cluster in the Drosophila oocyte provides an accessible model to address these questions, which Mohit Prasad and colleagues (p. 3692) have exploited to analyse the role of the Pak3 kinase. The authors find that Pak3 depletion in migrating border cells impairs migration – likely due to defects in the direction, length and stability of the protrusions extended by the border cells. These data suggest that forward-rear polarisation of the cluster is impaired. However, there are also severe defects in apicobasal polarity, and the authors define a signalling cascade involving Rac1, Pak3 and the JNK pathway, which regulates the apicobasal localisation of polarity proteins. As well as identifying another important player regulating collective cell migration, these data suggest an intriguing link between forward-rear and apicobasal polarity, which has yet to be investigated further.