Abstract
BackgroundThe assembly of the Drosophila embryo mitotic spindle during prophase depends upon a balance of outward forces generated by cortical dynein and inward forces generated by kinesin-14 and nuclear elasticity. Myosin II is known to contribute to the dynamics of the cell cortex but how this influences the prophase force-balance is unclear.Principal FindingsHere we investigated this question by injecting the myosin II inhibitor, Y27632, into early Drosophila embryos. We observed a significant increase in both the area of the dense cortical actin caps and in the spacing of the spindle poles. Tracking of microtubule plus ends marked by EB1-GFP and of actin at the cortex revealed that astral microtubules can interact with all regions of these expanded caps, presumably via their interaction with cortical dynein. In Scrambled mutants displaying abnormally small actin caps but normal prophase spindle length in late prophase, myosin II inhibition produced very short spindles.ConclusionsThese results suggest that two complementary outward forces are exerted on the prophase spindle by the overlying cortex. Specifically, dynein localized on the mechanically firm actin caps and the actomyosin-driven 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.
Highlights
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
These results suggest that two complementary outward forces are exerted on the prophase spindle by the overlying cortex
To test the hypothesis that myosin II plays a role in spindle dynamics, we microinjected a specific Rho kinase inhibitor, Y27632, into Drosophila syncytial embryos expressing GFP-tubulin
Summary
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. Myosin II has recently been reported to exert force on the spindle poles during prophase, presumably via a drag on cortex-anchored astral microtubules subsequent to nuclear envelope breakdown (NEB) through myosin-powered cortical flow [2]. 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]. Myosin II is known to contribute to the dynamics of the cell cortex but how this influences the prophase force-balance is unclear
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