ABSTRACT
Several cell motility processes including cytokinesis and cell locomotion are dependent on the interplay of the microtubule and actomyosin cytoskeletons. However, because such processes are essentially visual phenomena, interactions between the two cytoskeletal systems have been difficult to study quantitatively. To overcome this difficulty, we have developed the Xenopus oocyte as an inducible, quantitative model system for actomyosin-based cortical flow and then exploited the strengths of this system to assess the relationship between microtubules and cortical flow. As in other systems, oocyte cortical flow entails: (1) redistribution of cortical filamentous actin (f-actin); (2) a requirement for actomyosin; (3) redistribution of cell surface proteins; (4) a requirement for cell surface protein mobility; and (5) directed movement of cortical organelles. Cortical flow rate in the oocyte system is inversely proportional to the level of polymeric tubulin and microinjection of free tubulin has no effect on the rate of cortical flow. Enhancement of microtubule polymerization inhibits cortical f-actin cable formation during cortical flow. The effects of microtubule depolymerization on cortical flow are rapid, independent of transcription or translation, independent of effects on the oocyte intermediate filament system, and independent of the upstream stimulus for cortical flow. The results show that the microtubules themselves, or a factor associated with them, suppress cortical flow, either by mechanically resisting flow, or by modulating the actomyosin cytoskeleton.
Cortical contraction should not be confused with ‘cortical rotation’, a process whereby dorso-ventral polarity is established in the early amphibian embryo (Ubbels et al., 1983). In cortical contraction, the cortex moves toward the animal pole within 4-10 minutes of fertilization whereas in cortical rotation, the interior of the fertilized egg rotates with respect to the cortex 20-40 minutes after fertilization (Ubbels et al., 1983). Cortical contraction is actomyosin dependent (Ezzell et al., 1985), whereas cortical rotation appears to be driven by microtubules (Elinson and Rowning, 1988), and is actually stimulated by disruption of the actin cytoskeleton (Manes et al., 1978).
