The molecular motor dynein localises to kinetochores to establish kinetochore–microtubule attachments in early mitosis. Dynein is recruited to kinetochores with the help of two pathways: one that comprises the Rod–Zw10–Zwilch (RZZ) complex and the coiled-coil protein spindly, and another that involves the paralogs NudE and NudEL. The latter two proteins are ubiquitous dynein co-factors that are involved in numerous dynein-mediated processes, such as organelle transport, centrosome positioning and spindle assembly. In this issue, Reto Gassmann and co-workers dissect the role of the C. elegans NudE-homologue NUD-2 in early embryos (jcs212159). The authors find that NUD-2 is dispensable for dynein-dependent spindle assembly, and recruited to kinetochores independently of RZZ–spindly and dynein through the CENP-F-like proteins HCP1 and HCP-2. The absence of NUD-2 in embryos leads to delays in microtubule-attachment and the appearance of chromatin bridges during anaphase. Further, the spindle assembly checkpoint (SAC) is required for survival in the absence of NUD-2. Whereas dynein levels at kinetochores are diminished upon loss of NUD-2, SAC proteins are excessively recruited to kinetochores. Interestingly, this SAC signalling extends the duration of mitosis and decreases chromosome mis-segregation without NUD-2. This work demonstrates an essential function of NUD-2 for dynein at kinetochores in early embryonic development.
