During Drosophila melanogaster oogenesis, border cell clusters detach from the follicular epithelium of the egg chamber and migrate collectively towards the oocyte. Although collective cell migration requires polarized actomyosin contractility, the mechanisms regulating this process are not fully elucidated. Majumder et al. now show that the Par-1 cell polarity kinase spatially controls myosin-II (Myo-II) activity for correct border cell migration (Curr. Biol. 22, 363–372; 2012).

Par-1 was previously shown to impair border cell protrusions and detachment from the epithelium. The authors observed similar defects in border cell clusters deficient for Myo-II, and established that Par-1 increases the levels of active Myo-II in border cells. This was shown to occur indirectly through the Par-1-mediated phosphorylation and inactivation of myosin phosphatase, which normally inhibits Myo-II. Par-1 is known to localize to the rear of the border cell cluster. This spatial restriction was shown here to result in local inhibition of myosin phosphatase and a concurrent increase of Myo-II activity at the same site. The authors propose that the Par-1-mediated spatial enhancement of Myo-II activity and subsequent polarized cell contraction are crucial for cell detachment and collective migration. These findings link cell polarity to the control of actomyosin contractility, and shed light on the regulatory networks influencing collective cell migration.