In most animal cells, microtubules are focused on the centrosome, an organelle near the nucleus that organizes the microtubule cytoskeleton into a radial array. As a result, they exhibit a property known as `dynamic instability', involving continuous growth and shortening at their plus ends (away from the centrosome). Removal of the centrosome can cause a shift from dynamic instability to a behaviour called `treadmilling', in which the uncapped minus ends are continuously depolymerized, leading to an increase in the concentration of microtubule monomer that gives rise to persistent growth at plus ends. Treadmilling occurs when the rate of plus-end growth matches that of minus-end shortening.

In terminally differentiated cells, such as neurons and polarized epithelial cells, the microtubule cytoskeleton is not focused on the centrosome. However, these microtubules do not treadmill but rather tend to exhibit dynamic instability. For example, microtubules in neuronal axons grow in vivo from their plus ends only, despite the fact that their minus ends are released from the centrosome. This has led to the proposal that such microtubules are stabilized by other putative factors, such as cytoplasmic g-tubulin.

Cell–cell contacts are crucial to the functions of neuronal and epithelial cells, and the formation of such contacts induces cell polarization. On page 797 of this issue, Chausovsky et al. show that the minus ends of microtubules are stabilized by signalling from cadherins, the adhesion receptors of adherens-type cell junctions. This regulation of microtubule dynamics would allow the establishment and maintenance of cell polarization by ensuring that microtubules remain stable when released from the centrosome. Expression of cadherins can initiate cell contact and polarization in normally solitary cells, and the authors used Chinese hamster ovary (CHO) cells expressing E- or N-cadherin to monitor the effects of these receptors on microtubule organization in cells and in centrosome-free cytoplasts. They found that cadherin expression prevents the reduction in microtubule density that normally accompanies removal of the centrosome in fibroblasts. The picture shows the distribution of microtubules (red) in a CHO cell expressing N-cadherin (the centrosome is shown in green).

Chausovsky and colleagues propose that cadherins initiate a signalling pathway that influences microtubule dynamics by stabilizing minus ends, preventing treadmilling and thereby allowing net elongation. It seems that, although this signalling is direct, expression of cadherins per se is not sufficient for microtubule stabilization. Instead, cell–cell contacts, of which cadherins are an integral part, must be present for this process to occur. This would ensure that as cells form contacts with their neighbours, they are able to relinquish their radial microtubule arrays whilst still retaining sufficient amounts of microtubule polymer.