Nocodazole treatment to remove dynamic microtubules (below) reveals stable microtubules (arrowhead) that deliver centralspindlin to the equatorial cortex, activating myosin II (lavender).
The cleavage furrow forms at the equatorial region of the cell, when the underlying cortex transiently accumulates active myosin II that pulls on cortical actin filaments, constricting the membrane. It's clear that positioning the furrow is one job of the mitotic apparatus, and probably its microtubules, but exactly how has been a mystery. To investigate this, von Dassow and Foe looked at microtubule dynamics and active myosin II distribution at various points during cytokinesis. They found that just prior to cleavage, the entire cortex was transiently depleted of activated myosin, setting the stage for its focused repositioning later on. Then, during anaphase, a set of stable microtubules formed, stretching from the centrosome to the equator, while short-lived dynamic microtubules spread to contact other regions of the cortex. Active myosin accumulated only where the stable microtubules contacted the cortex. The factors responsible for stability of the equatorial microtubules are not yet known.
These results were accounted for in a computer model by Odell and Foe when both types of microtubules bound centralspindlin, a complex of kinesin motor and Rho modulators that assembles on microtubules and motors toward the cortex. The stable microtubules acted as long-lasting rails, allowing time for centralspindlin to reach the cortex and activate myosin II. Meanwhile, excess centralspindlin remained sequestered on dynamic microtubules, but couldn't reach the cortex before those microtubules depolymerized, thus reducing contractility everywhere else.
