Actin dynamics must play an important role in centrosome separation based on the observations that separation is incomplete in embryos treated with cytochalasin D [18] and that actin polymerization is crucial for the centrosome separation before NEB [19], but details of this cortex-to-spindle opinions and myosin II involvement were not studied

Actin dynamics must play an important role in centrosome separation based on the observations that separation is incomplete in embryos treated with cytochalasin D [18] and that actin polymerization is crucial for the centrosome separation before NEB [19], but details of this cortex-to-spindle opinions and myosin II involvement were not studied. The question about the nature of the spindle-cortex interaction is intimately linked to another outstanding question C the relation between the internal and external forces shaping the spindle [20]. contraction of the deformable soft patches of the actin cortex, cooperate to pull astral microtubules outward. Thus, myosin II controls the size and dynamic properties of the actin-based cortex to influence the spacing of the poles of the underlying spindle during prophase. Introduction Microtubule (MTs) and actin-myosin arrays interact and cooperate in many mechanochemical modules of cell motility and cell division [1] but the functional implications of such interactions are not well understood. In particular, interactions of mitotic spindles with the F-actin cortex are crucial for spindle positioning and orientation [2]C[4] as well as the regulation of cytokinesis [5], yet whether the actin-myosin network affects internal processes of mitotic Resminostat hydrochloride spindle assembly and maintenance, or only external phenomena involving the spindle’s interactions with other regions of the cell such as the cortex, is still a controversial question Resminostat hydrochloride [4]. Some evidence suggests that myosin II is needed only for cytokinesis: inhibition of myosin II in Resminostat hydrochloride echinoderm blastomeres blocks cytokinesis but not mitosis [6]; similarly, RNAi depletion of myosin II in S2 cells blocks cytokinesis but metaphase and anaphase spindles are morphologically normal [7]. On the other hand, myosin II has recently been reported to exert pressure around the spindle poles during prophase, presumably via a drag on cortex-anchored astral microtubules subsequent to nuclear envelope breakdown (NEB) through myosin-powered cortical circulation [2]. In locust spermatocytes, there is evidence that actin and myosin are involved in anaphase chromosome movement [8]. Curiously, it was recently reported that F-actin promotes spindle lengthening, perhaps by interactions with astral MTs, while Myosin-10 works antagonistically to shorten the spindle [9]. The early embryo is a very convenient system for investigating the coupling between the spindle and the actomyosin cortex because of this organism’s amenability to genetic analysis, inhibitor microinjection and microscopy [10]. In early embryogenesis, some morphogenetic events such as cellularization [11] and nuclear migration [12] indicate interactions between the actomyosin cytoskeleton and microtubule arrays; myosin II is usually thought to have additional as yet unidentified functions [13]. Following our earlier efforts [14], here we focus on the syncytial blastoderm divisions that occur at the cortex of the embryo, just beneath the plasma membrane, where dramatic redistribution of the cortical actin accompanies spindle morphogenesis [15]. In these cycles, actin Resminostat hydrochloride concentrates into caps centered above each nucleus and centrosomes. As the nuclei progress into prophase, the centrosomes migrate toward reverse poles and the caps expand in synchrony with the centrosomes [14]. After NEB, a transient constant state is usually reached in prophase, after which the centrosomes individual and the spindle elongates further. Here, we concentrate on the early stage of mitosis C prophase C because myosin-dependent contraction of the cortex has been reported at this stage, while at prometaphase myosin concentration starts to decline rapidly throughout the cortex [16]. The role of myosin II in cellularization [11] and the influence of astral MT arrays around the quick spatial reorganizations of the actomyosin cortex [15], [17] are well documented. Actin dynamics must play an important role in centrosome separation based on the observations that separation is Rabbit Polyclonal to PEX3 incomplete in embryos treated with cytochalasin D [18] and that actin polymerization is crucial for the centrosome.