Kinetochores establish the site where spindle microtubules attach to chromosomes, and are also the site of spindle assembly checkpoint (SAC) activity. By using the SAC, kinetochores that are unattached to chromosomes form an inhibitor complex that delays the onset of anaphase. This delay helps to avoid aneuploidy (an abnormal number of chromosomes within cells) as it extends the time available to establish correct kinetochore–microtubule linkages. Formation of the inhibitor complex is dependent on Mad1, a kinetochore-bound receptor that binds Mad2 and facilitates its interaction with Cdc20 to form an essential part of this complex. But whether Mad1 has any additional mitotic function is unknown. On page , Roger Karess and colleagues show that Mad1 – independently of its interaction with Mad2 – promotes correct kinetochore–microtubule linkages during mitosis. By studying the impact of a mad1-null mutation in Drosophila melanogaster, the authors show that aneuploidy is as infrequent in mad1 mutants as it is in wild-type or mad2 mutant flies. However, live-cell imaging reveals that these mutants do display defects in anaphase that are not found in mad2 mutants and are characterised by the presence of lagging kinetochores, some of which are caused by merotelic linkages (i.e. when a single kinetochore attaches to both poles of the spindle). The authors, therefore, conclude that Mad1, unlike Mad2, has a dual role in coordinating the proper functioning of mitosis.
