Cortical actin dynamics facilitate early-stage centrosome separation.

Proper centrosome separation is a prerequisite for positioning the bipolar spindle. Although studies demonstrate that microtubules (MTs) and their associated motors drive centrosome separation [1], the role of actin in centrosome separation remains less clear. Studies in tissue culture cells indicate that actin- and myosin-based cortical flow is primarily responsible for driving late centrosome separation [2], whereas other studies suggest that actin plays a more passive role by serving as an attachment site for astral MTs to pull centrosomes apart [3-6]. Here we demonstrate that prior to nuclear envelope breakdown (NEB) in Drosophila embryos, proper centrosome separation does not require myosin II but requires dynamic actin rearrangements at the growing edge of the interphase cap. Both Arp2/3- and Formin-mediated actin remodeling are required for separating the centrosome pairs before NEB. The Apc2-Armadillo complex appears to link cap expansion to centrosome separation. In contrast, the mechanisms driving centrosome separation after NEB are independent of the actin cytoskeleton and compensate for earlier separation defects. Our studies show that the dynamics of actin polymerization drive centrosome separation, and this has important implications for centrosome positioning during processes such as cell migration [7, 8], cell polarity maintenance [9, 10], and asymmetric cell division [11, 12].