The spindle checkpoint senses whether chromosomes are properly attached to the spindle and delays the onset of anaphase until they are. Several proteins involved in the checkpoint, for example Mad2, localize at kinetochores of unattached chromosomes and become lost from the kinetochores of properly attached chromosomes, providing a possible mechanism for linking kinetochore attachment to the cell-cycle machinery. But how are checkpoint proteins lost from properly attached kinetochores? When a chromosome is properly attached to the spindle, sister kinetochores are attached by microtubule bundles to opposing spindle poles, producing tension on the kinetochores. Loss of checkpoint proteins could be triggered either by tension on the kinetochore, or by microtubule occupancy at the kinetochore. There are conflicting reports about which of these two factors is responsible, but a recent paper [1xCheckpoint signals in grasshopper meiosis are sensitive to microtubule attachment, but tension is still essential. Nicklas, R.B et al. J. Cell Sci. 2001; 114: 4173–4183PubMedSee all References[1] provides a possible way to reconcile the dispute.Nicklas and colleagues used micromanipulation in grasshopper spermatocytes to generate three types of kinetochores: unattached kinetochores that had no associated microtubules and experienced no tension, fully attached kinetochores in which sister kinetochores were attached to opposing poles and thus experienced both tension and high microtubule occupancy, and ‘weakly attached’ kinetochores, in which one kinetochore was attached to a pole, while the other was either unattached or attached to the same pole. These ‘weakly attached’ kinetochores had microtubules occupying the kinetochore region but experienced no tension because there was no opposing force on the other kinetochore and because, unlike vertebrate cells, there is no polar ejection force in insect spermatocytes. Significantly, these weakly attached kinetochores lost checkpoint proteins, unlike the unattached kinetochores. Because the tension is the same (zero) both for weakly attached and unattached chromosomes, tension must not be required for loss of checkpoint proteins. Instead, the key appears to be microtubule occupancy, which is the only difference between an unattached and a weakly attached kinetochore.However, loss of checkpoint proteins at weakly attached kinetochores was not as complete as the loss from fully attached kinetochores, so tension clearly has some effect. Weakly attached kinetochores were found to have fewer microtubules associated with them than fully attached kinetochores under tension. Hence, tension might act indirectly, by increasing microtubule occupancy, which is then sensed by the checkpoint machinery.But how does increased microtubule occupancy lead to a loss of checkpoint proteins from the kinetochore? It is now known that cytoplasmic dynein is able to move checkpoint proteins from the kinetochore to the spindle poles. If checkpoint proteins are continuously loaded onto kinetochores at a fixed rate, and constantly removed by transport along microtubules, then the steady-state concentration of checkpoint proteins at the kinetochore should be roughly proportional to the number of microtubules. Lack of tension on improperly attached chromosomes causes loss of kinetochore microtubules, leading to a build-up of checkpoint proteins at the kinetochore. This just leaves one big question, how does tension affect microtubule occupancy?